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1.	Altena, Renske, et al. (author) Current status of contemporary diagnostic radiotracers in the management of breast cancer : first steps toward theranostic applications 2023 In: EJNMMI Research. - : Springer Nature. - 2191-219X. ; 13:1 Research review (peer-reviewed)abstract BackgroundExpanding therapeutic possibilities have improved disease-related prospects for breast cancer patients. Pathological analysis on a tumor biopsy is the current reference standard biomarker used to select for treatment with targeted anticancer drugs. This method has, however, several limitations, related to intra- and intertumoral as well as spatial heterogeneity in receptor expression as well as the need to perform invasive procedures that are not always technically feasible.Main bodyIn this narrative review, we focus on the current role of molecular imaging with contemporary radiotracers for positron emission tomography (PET) in breast cancer. We provide an overview of diagnostic radiotracers that represent treatment targets, such as programmed death ligand 1, human epidermal growth factor receptor 2, polyadenosine diphosphate-ribose polymerase and estrogen receptor, and discuss developments in therapeutic radionuclides for breast cancer management.ConclusionImaging of treatment targets with PET tracers may provide a more reliable precision medicine tool to find the right treatment for the right patient at the right time. In addition to visualization of the target of treatment, theranostic trials with alpha- or beta-emitting isotopes provide a future treatment option for patients with metastatic breast cancer.
2.	Altena, Renske, et al. (author) Human Epidermal Growth Factor Receptor 2 (HER2) PET Imaging of HER2-Low Breast Cancer with [ 68 Ga]Ga-ABY-025 : Results from a Pilot Study 2024 In: Journal of Nuclear Medicine. - : Society of Nuclear Medicine and Molecular Imaging. - 0161-5505 .- 1535-5667. ; 65:5, s. 700-707 Journal article (peer-reviewed)abstract Patients with HER2-low metastatic breast cancer (mBC), defined as an immunohistochemistry (IHC) score of 1+ or 2+ without HER2 gene amplification, may benefit from HER2 antibody-drug conjugates. Identifying suitable candidates is a clinical challenge because of spatial and temporal heterogeneity in HER2 expression and discrepancies in pathologic reporting. We aimed to investigate the feasibility and safety of HER2-specific PET imaging with [ 68 Ga]Ga-ABY-025 for visualization of HER2-low mBC.Methods: A prospective pilot study was done with 10 patients who had HER2-low mBC, as part of a phase 2 basket imaging study with [ 68 Ga]Ga-ABY-025 in HER2-expressing solid tumors. Patients were recruited at the Breast Clinic at the Karolinska University Hospital, Stockholm, Sweden. PET/CT images were acquired 3 h after injection of 200 MBq of [ 68 Ga]Ga-ABY-025. The SUV max was used to quantify tracer uptake. Ultrasound-guided tumor biopsies were guided by results from the HER2 PET. The main outcome-the safety and feasibility of HER2 PET in patients with HER2low mBC, measured the occurrence of possible procedure -related adverse events.Results: Ten patients with HER2-low mBC underwent [ 68 Ga]Ga-ABY-025 PET/CT with paired tumor biopsies. No adverse events occurred. In all patients, [ 68 Ga]Ga-ABY-025-avid lesions with substantial intra- and interindividual heterogeneity in tracer uptake were noted. In 8 of 10 patients with ABY-025-avid lesions, the HER2low status of the corresponding lesions was confirmed by IHC or in situ hybridization. Two patients had an IHC score of 0 in the tumor biopsies:1 in a cutaneous lesion with a low SUV max and 1 in a liver metastasis with a high SUV max but a "cold" core.Conclusion: The visualization of HER2-low mBC with [ 68 Ga]Ga-ABY-025 PET/CT was feasible and safe. Areas of tracer uptake showed varying levels of HER2 expression on IHC. The observed intra- and interindividual heterogeneity in [ 68 Ga]Ga-ABY-025 uptake suggested that HER2 PET might be used as a tool for the noninvasive assessment of disease heterogeneity and has the potential to identify patients in whom HER2-targeted drugs can have a clinical benefit.
3.	Alvehus, Malin, et al. (author) Adipose tissue IL-8 is increased in normal weight women after menopause and reduced after gastric bypass surgery in obese women 2012 In: Clinical Endocrinology. - : Wiley-Blackwell. - 0300-0664 .- 1365-2265. ; 77:5, s. 684-690 Journal article (peer-reviewed)abstract Objective: The menopausal transition is characterized by increased body fat accumulation, including redistribution from peripheral to central fat depots. This distribution is associated with an increased risk of type 2 diabetes and cardiovascular disease which are linked to low-grade inflammation. We determined whether postmenopausal women have higher levels of inflammatory markers, compared to premenopausal women. We also wanted to determine if these markers are reduced by stable weight loss in obese women. Design and methods: Anthropometric data, blood samples, and subcutaneous adipose tissue biopsies were collected from normal weight premenopausal and postmenopausal women and obese women before and 2 years after gastric bypass surgery. Serum protein levels and adipose tissue gene expression of inflammatory markers were investigated. Results: IL-8 expression in adipose tissue and circulating levels were higher in postmenopausal versus premenopausal women. IL-8 expression was associated with waist circumference, independent of menopausal status. IL-6 expression and serum levels of monocyte chemoattractant protein (MCP)-1 were higher in postmenopausal versus premenopausal women. Two years after gastric bypass surgery, adipose expression of IL-8, tumor necrosis factor-α, and MCP-1 decreased significantly. Serum insulin levels were associated with inflammation-related gene expression before gastric bypass surgery, but these associations disappeared after surgery. Conclusion: Postmenopausal women have an increased inflammatory response in the subcutaneous fat and circulation. Inflammatory markers in adipose tissue decreased significantly after surgery-induced weight loss. This effect may be beneficial for metabolic control and reduced cardiovascular risk after weight loss. © 2011 Blackwell Publishing Ltd.
4.	Alvehus, Malin, et al. (author) Decreased TLR4 and Increased MIF Adipose Gene Expression Following Long-Term Diet Intervention Other publication (other academic/artistic)
5.	Alvehus, Malin, et al. (author) Metabolic adaptations in skeletal muscle, adipose tissue, and whole-body oxidative capacity in response to resistance training 2014 In: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 114:7, s. 1463-1471 Journal article (peer-reviewed)abstract The effects of resistance training on mitochondrial biogenesis and oxidative capacity in skeletal muscle are not fully characterized, and even less is known about alterations in adipose tissue. We aimed to investigate adaptations in oxidative metabolism in skeletal muscle and adipose tissue after 8 weeks of heavy resistance training in apparently healthy young men. Expression of genes linked to oxidative metabolism in the skeletal muscle and adipose tissue was assessed before and after the training program. Body composition, peak oxygen uptake (VO2 peak), fat oxidation, activity of mitochondrial enzyme in muscle, and serum adiponectin levels were also determined before and after resistance training. In muscle, the expression of the genes AdipoR1 and COX4 increased after resistance training (9 and 13 %, respectively), whereas the expression levels of the genes PGC-1 alpha, SIRT1, TFAM, CPT1b, and FNDC5 did not change. In adipose tissue, the expression of the genes SIRT1 and CPT1b decreased after training (20 and 23 %, respectively). There was an increase in lean mass (from 59.7 +/- A 6.1 to 61.9 +/- A 6.2 kg), VO2 peak (from 49.7 +/- A 5.5 to 56.3 +/- A 5.0 ml/kg/min), and fat oxidation (from 6.8 +/- A 2.1 to 9.1 +/- A 2.7 mg/kg fat-free mass/min) after training, whereas serum adiponectin levels decreased significantly and enzyme activity of citrate synthase and 3-hydroxyacyl-CoA dehydrogenase did not change. Despite significant increases in VO2 peak, fat oxidation, and lean mass following resistance training, the total effect on gene expression and enzyme activity linked to oxidative metabolism was moderate.
6.	Alvehus, Malin, et al. (author) The human visceral fat depot has a unique inflammatory profile 2010 In: Obesity. - : Nature Publishing Group. - 1930-7381 .- 1930-739X. ; 18:5, s. 879-883 Journal article (peer-reviewed)abstract Obesity can be considered as a low-grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity-associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3 +/- 5.5 kg/m2) were included in the study. Body fat (dual-energy X-ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation-related differences in gene expression(real-time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation,while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01)expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.
7.	Andersson, Therése, 1978- (author) Estrogen and Glucocorticoid Metabolism 2010 Doctoral thesis (other academic/artistic)abstract Background: Cardiovascular disease (CVD) is the leading cause of death among women in Sweden. The risk of CVD increases rapidly after the menopause. A major contributing factor may be the redistribution of adipose tissue, from the peripheral to central depots, associated with menopause. This change in body composition is commonly attributed to declining estrogen levels but may also be affected by tissue-specific alterations in exposure to other steroid hormones, notably glucocorticoids – mainly cortisol in humans. Indeed, adipose tissue-specific overexpression of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) induces central obesity, insulin resistance and hypertension in mice. Interestingly, estrogen may regulate this enzyme. The aim of this thesis was to investigate putative links between estrogen and glucocorticoid activation by 11βHSD1. Materials and Methods: 11βHSD1 expression and/or activity in adipose tissue and liver, and adipose estrogen receptor α and β (ERα and ERβ) gene expression, were investigated in lean pre- and postmenopausal women and ovariectomized rodents with and without estrogen supplementation. In lean women measures of 11βHSD1 were correlated to risk markers for CVD. The association between adipose 11βHSD1 and ER mRNA expression was investigated in both lean women and rats and in an additional cohort of obese premenopausal women. In vitro experiments with adipocyte cell lines were used to explore possible pathways for estrogen regulation of 11βHSD1. Results: Subcutaneous adipose tissue transcript levels and hepatic activity of 11βHSD1 were higher in postmenopausal vs. premenopausal women. In rodents, estrogen treatment to ovariectomized rats decreased visceral adipose tissue 11βHSD1, resulting in a shift towards higher subcutaneous (vs. visceral) 11βHSD1 mRNA expression/activity. Increased adipose and hepatic 11βHSD1 were associated with increased blood pressure and a disadvantageous blood lipid profile in humans. We found significant positive associations between 11βHSD1 and ERβ transcript levels in adipose tissue. The in vitro experiments showed upregulation of 11βHSD1 mRNA expression and activity with estrogen or ERβ-agonist treatment at low (corresponding to physiological) concentrations. Conclusions: Our studies show for the first time increased local tissue glucocorticoid activation with menopause/age in women. This may contribute to an increased risk of CVD. Estrogen treatment in rodents induces a shift in 11βHSD1 activity towards the subcutaneous adipose tissue depots, which may direct fat accumulation to this metabolically “safer” depot. The in vitro studies suggest that low-dose estrogen treatment upregulates 11βHSD1 via ERβ. In summary, estrogen - glucocorticoid metabolism interactions may be key in the development of menopause-related metabolic dysfunction and in part mediate the beneficial effects of postmenopausal estrogen treatment on body fat distribution.
8.	Andersson, Therése, 1978-, et al. (author) Tissue-specific increases in 11beta-hydroxysteroid dehydrogenase type 1 in normal weight postmenopausal women 2009 In: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 4:12, s. e8475- Journal article (peer-reviewed)abstract With age and menopause there is a shift in adipose distribution from gluteo-femoral to abdominal depots in women. Associated with this redistribution of fat are increased risks of type 2 diabetes and cardiovascular disease. Glucocorticoids influence body composition, and 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) which converts inert cortisone to active cortisol is a putative key mediator of metabolic complications in obesity. Increased 11betaHSD1 in adipose tissue may contribute to postmenopausal central obesity. We hypothesized that tissue-specific 11betaHSD1 gene expression and activity are up-regulated in the older, postmenopausal women compared to young, premenopausal women. Twenty-three pre- and 23 postmenopausal, healthy, normal weight women were recruited. The participants underwent a urine collection, a subcutaneous adipose tissue biopsy and the hepatic 11betaHSD1 activity was estimated by the serum cortisol response after an oral dose of cortisone. Urinary (5alpha-tetrahydrocortisol+5beta-tetrahydrocortisol)/tetrahydrocortisone ratios were higher in postmenopausal women versus premenopausal women in luteal phase (P<0.05), indicating an increased whole-body 11betaHSD1 activity. Postmenopausal women had higher 11betaHSD1 gene expression in subcutaneous fat (P<0.05). Hepatic first pass conversion of oral cortisone to cortisol was also increased in postmenopausal women versus premenopausal women in follicular phase of the menstrual cycle (P<0.01, at 30 min post cortisone ingestion), suggesting higher hepatic 11betaHSD1 activity. In conclusion, our results indicate that postmenopausal normal weight women have increased 11betaHSD1 activity in adipose tissue and liver. This may contribute to metabolic dysfunctions with menopause and ageing in women.
9.	B. Nutley, Sissela, et al. (author) COVID-19 Restrictions Resulted in Both Positive and Negative Effects on Digital Media Use, Mental Health, and Lifestyle Habits 2023 In: International Journal of Environmental Research and Public Health. - 1660-4601. ; 20:6 Journal article (peer-reviewed)abstract While studies have reported effects on digital media during the COVID-19 restrictions, few have included data prior to the pandemic, and most have only measured screen time. We therefore investigated changes in specific digital media activities, as well as mental health and lifestyle habits, in a longitudinal study of adolescents spanning from before the pandemic (T1) to one month into restrictions (T2) and one year later when schools had reopened (T3). Adolescents (16–19 years) rated smartphone use, problematic/addictive media use, negative experiences (e.g., victimization), mental health (i.e., irritability, stress, and closeness), and protective lifestyle habits (i.e., sleep and exercise). Results showed initial decreases in irritability and negative digital experiences, increases in sleep and exercise, as well as a decrease in closeness during remote learning (T2). However, these changes returned to, or superseded, their initial levels at follow-up (T3). There were also increases in digital media use and stress at T3. Conclusively, by investigating specific digital media activities and collecting data both prior to and during different phases of the pandemic, we were able to find both positive and negative effects.
10.	Blomquist, Caroline, et al. (author) Attenuated Low-Grade Inflammation Following Long-Term Dietary Intervention in Postmenopausal Women with Obesity 2017 In: Obesity. - : Wiley. - 1930-7381 .- 1930-739X. ; 25:5, s. 892-900 Journal article (peer-reviewed)abstract ObjectiveAbdominal fat accumulation after menopause is associated with low-grade inflammation and increased risk of metabolic disorders. Effective long-term lifestyle treatment is therefore needed. MethodsSeventy healthy postmenopausal women (age 605.6 years) with BMI 32.55.5 were randomized to a Paleolithic-type diet (PD) or a prudent control diet (CD) for 24 months. Blood samples and fat biopsies were collected at baseline, 6 months, and 24 months to analyze inflammation-related parameters. ResultsAndroid fat decreased significantly more in the PD group (P=0.009) during the first 6 months with weight maintenance at 24 months in both groups. Long-term significant effects (P<0.001) on adipose gene expression were found for toll-like receptor 4 (decreased at 24 months) and macrophage migration inhibitory factor (increased at 24 months) in both groups. Serum interleukin 6 (IL-6) and tumor necrosis factor levels were decreased at 24 months in both groups (P<0.001) with a significant diet-by-time interaction for serum IL-6 (P=0.022). High-sensitivity C-reactive protein was decreased in the PD group at 24 months (P=0.001). ConclusionsA reduction of abdominal obesity in postmenopausal women is linked to specific changes in inflammation-related adipose gene expression.
11.	Boman, Niklas, 1984- (author) Building muscle : a translation of training adaptation 2016 Doctoral thesis (other academic/artistic)abstract Training is preparation for what is expected to come through utilization of the plastic and resistive features of nature, known as adaptation. As such, training in humans may have a number of desired goals. These are typically related to sports performance or education. Whatever the goal, a plan needs to be made for reaching it. One needs to identify or select which activities and environments constitute the event or events to which adaptation is sought. Adaptations occurs by imposing something similar to said environment and practicing the selected activities in preparation for the events that can ultimately lead to goal fulfillment.One quite common goal of physical training is to achieve a more lean and muscular physique, be it for reasons of performance or esthetics. A leaner and more muscular physique can have many advantages for health and quality of life. If we are to prepare the body’s physical capabilities and properties, they should be utilized in the preparation. By proper design and execution of a program for physical preparation, we set out on the path to achieve the goal.A factor that is often highlighted as an important key to building muscle in the human body is the steroid hormone testosterone. According to the hormone hypothesis, increases in muscle mass are achieved through transient elevations in anabolic hormones, such as testosterone and IGF1, induced by physical training. To achieve hypertrophy of the muscles through physical training, one must ensure sure that the muscles get the correct signal, the growth signal, as a result of the training.The work presented in this thesis is, in part, an examination of the hormone hypothesis, with both empirical and theoretical elements. The empirical foundations are results of an experiment in which a group of young men were subjected to a program of physical training, designed for all intents and purposes in accordance with contemporary knowledge, to result in muscular hypertrophy in the subjects. The goal was achieved, with an average 4.6% increase in lean body mass in the subjects after the training program. However, there was no evidence that anabolic hormones were elevated at any time during the measurement period.The major part of this thesis details a model for explaining the collected observations. It is not intended to merely provide a guide for achieving a leaner more muscular physique but rather is aimed at formulating the problem of inducing the desired adaptations and difficulties involved in approaching the problem. For reasons discussed in this thesis, I do not claim that this is the full and final word on the matter. However, it goes some way toward explaining why, and perhaps how, desired goals should be formulated so that the muscles may understand them.
12.	Boman, Niklas, et al. (author) Effects of protein ingestion on the hormonal response to resistance exercise and increases in lean body mass after eight weeks of training Other publication (other academic/artistic)
13.	Boman, Niklas, et al. (author) Gene expression and fiber type variations in repeated vastus lateralis biopsies 2015 In: Muscle and Nerve. - : Wiley. - 0148-639X .- 1097-4598. ; 52:2, s. 812-817 Journal article (peer-reviewed)abstract Introduction: Muscle sample collection can introduce variation in any measured variable due to inter- and intramuscle variation. We investigated the variation in gene expression and fiber type composition after repeated biopsy sampling from the vastus lateralis muscle. Methods: Six subjects donated 3 tissue samples each. One hour after baseline sampling from 1 vastus lateralis muscle, samples from both vastus lateralis muscles were obtained. Results: The fiber type composition differed between biopsies taken from the same leg. There were no within-subject differences in gene expression between the 3 biopsies. Multivariate analysis supports a model in which gene expression differs significantly between individuals but is not affected by repeated muscle biopsy sampling from the same subject. Conclusion: One vastus lateralis muscle sample per subject is sufficient to establish a reliable baseline for comparing gene expression representing selected pathways over time within the same individual.
14.	Burén, Jonas, et al. (author) A ketogenic low‐carbohydrate high‐fat diet increases ldl cholesterol in healthy, young, normal‐weight women : A randomized controlled feeding trial 2021 In: Nutrients. - : MDPI AG. - 2072-6643. ; 13:3, s. 1-12 Journal article (peer-reviewed)abstract Ketogenic low‐carbohydrate high‐fat (LCHF) diets are popular among young, healthy, normal‐weight individuals for various reasons. We aimed to investigate the effect of a ketogenic LCHF diet on low‐density lipoprotein (LDL) cholesterol (primary outcome), LDL cholesterol sub-fractions and conventional cardiovascular risk factors in the blood of healthy, young, and nor-mal‐weight women. The study was a randomized, controlled, feeding trial with crossover design. Twenty‐four women were assigned to a 4 week ketogenic LCHF diet (4% carbohydrates; 77% fat; 19% protein) followed by a 4 week National Food Agency recommended control diet (44% carbo-hydrates; 33% fat; 19% protein), or the reverse sequence due to the crossover design. Treatment periods were separated by a 15 week washout period. Seventeen women completed the study and treatment effects were evaluated using mixed models. The LCHF diet increased LDL cholesterol in every woman with a treatment effect of 1.82 mM (p < 0.001). In addition, Apolipoprotein B‐100 (ApoB), small, dense LDL cholesterol as well as large, buoyant LDL cholesterol increased (p < 0.001, p < 0.01, and p < 0.001, respectively). The data suggest that feeding healthy, young, normal‐weight women a ketogenic LCHF diet induces a deleterious blood lipid profile. The elevated LDL cholesterol should be a cause for concern in young, healthy, normal‐weight women following this kind of LCHF diet.
15.	Burén, Jonas, 1984, et al. (author) Adolescent girls’ cosmetic surgery consideration, parental appearance pressure, and materialism 2016 In: The 13th Nordic Youth Research Symposium (NYRIS), Trollhättan, 15-17 June. Conference paper (other academic/artistic)abstract During the last decade, there has been a dramatic increase in the number of cosmetic surgery procedures performed each year. Minimally invasive procedures, for example Botox and filler injections, have also increased markedly. Consequently, several international researchers have argued that there has been a shift toward a more liberal attitude to cosmetic surgery and especially among young people. Despite these trends, very few studies have examined the views that young people have of cosmetic surgery, their acceptance of changing the body by cosmetic surgery, or the predictors of cosmetic surgery consideration. In an ongoing study, we wish to shed light on some of these issues by examining attitudes toward cosmetic surgery, and the potential predictors of cosmetic surgery acceptance among young women. A total of 1148 adolescent girls, age 13-18, were recruited through the Internet. An online questionnaire, comprising questions about (for example) media and Internet use, self-esteem, body image, parental appearance pressure, cosmetic surgery, and materialistic values, was distributed. Analyses showed that 1/5 indicated that they might pursue cosmetic surgery in the future, and 1/3 stated that they would do cosmetic surgery if they got a procedure for free. The participants were generally in support of the notion of cosmetic surgery as an acceptable way to overcome poor self- or body-esteem. Analyses also showed that greater parental appearance pressure was associated with materialistic values. Both of these variables (parental appearance pressure and materialistic values) were significant predictors of adolescent girls cosmetic surgery acceptance, as well as of cosmetic surgery consideration. The above findings may be situated in both a developmental psychology- and sociocultural perspective.
16.	Burén, Jonas, et al. (author) Dexamethasone impairs insulin signalling and glucose transport by depletion of insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase B in primary cultured rat adipocytes. 2002 In: European Journal of Endocrinology. - : European Society of Endocrinology. - 0804-4643 .- 1479-683X. ; 146:3, s. 419-29 Journal article (peer-reviewed)abstract OBJECTIVE: Glucocorticoid excess leads to insulin resistance. This study explores the effects of glucocorticoids on the glucose transport system and insulin signalling in rat adipocytes. The interaction between glucocorticoids and high levels of insulin and glucose is also addressed.DESIGN AND METHODS: Isolated rat adipocytes were cultured for 24 h at different glucose concentrations (5 and 15 mmol/l) with or without the glucocorticoid analogue dexamethasone (0.3 micromol/l) and insulin (10(4) microU/ml). After the culture period, the cells were washed and then basal and insulin-stimulated glucose uptake, insulin binding and lipolysis as well as cellular content of insulin signalling proteins (insulin receptor substrate-1 (IRS-1), IRS-2, phosphatidylinositol 3-kinase (PI3-K) and protein kinase B (PKB)) and glucose transporter isoform GLUT4 were measured.RESULTS: Dexamethasone in the medium markedly decreased both basal and insulin-stimulated glucose uptake at both 5 and 15 mmol/l glucose (by approximately 40-50%, P<0.001 and P<0.05 respectively). Combined long-term treatment with insulin and dexamethasone exerted additive effects in decreasing basal, and to a lesser extent insulin-stimulated, glucose uptake capacity (P<0.05) compared with dexamethasone alone, but this was seen only at high glucose (15 mmol/l). Insulin binding was decreased (by approximately 40%, P<0.05) in dexamethasone-treated cells independently of surrounding glucose concentration. Following dexamethasone treatment a approximately 75% decrease (P<0.001) in IRS-1 expression and an increase in IRS-2 (by approximately 150%, P<0.001) was shown. Dexamethasone also induced a subtle decrease in PI3-K (by approximately 20%, P<0.01) and a substantial decrease in PKB content (by approximately 45%, P<0.001). Insulin-stimulated PKB phosphorylation was decreased (by approximately 40%, P<0.01) in dexamethasone-treated cells. Dexamethasone did not alter the amount of total cellular membrane-associated GLUT4 protein. The effects of dexamethasone per se on glucose transport and insulin signalling proteins were mainly unaffected by the surrounding glucose and insulin levels. Dexamethasone increased the basal lipolytic rate (approximately 4-fold, P<0.05), but did not alter the antilipolytic effect of insulin.CONCLUSIONS: These results suggest that glucocorticoids, independently of the surrounding glucose and insulin concentration, impair glucose transport capacity in fat cells. This is not due to alterations in GLUT4 abundance. Instead dexamethasone-induced insulin resistance may be mediated via reduced cellular content of IRS-1 and PKB accompanied by a parallel reduction in insulin-stimulated activation of PKB.
17.	Burén, Jonas, et al. (author) Effects of a ketogenic diet on body composition in healthy, young, normal-weight women : a randomized controlled feeding trial 2024 In: Nutrients. - : MDPI. - 2072-6643. ; 16:13 Journal article (peer-reviewed)abstract This study investigates the effects of a ketogenic low-carbohydrate high-fat (LCHF) diet on body composition in healthy, young, normal-weight women. With the increasing interest in ketogenic diets for their various health benefits, this research aims to understand their impact on body composition, focusing on women who are often underrepresented in such studies. Conducting a randomized controlled feeding trial with a crossover design, this study compares a ketogenic LCHF diet to a Swedish National Food Agency (NFA)-recommended control diet over four weeks. Seventeen healthy, young, normal-weight women adhered strictly to the provided diets, with ketosis confirmed through blood β-hydroxybutyrate concentrations. Dual-energy X-ray absorptiometry (DXA) was utilized for precise body composition measurements. To avoid bias, all statistical analyses were performed blind. The findings reveal that the ketogenic LCHF diet led to a significant reduction in both lean mass (−1.45 kg 95% CI: [−1.90;−1.00]; p < 0.001) and fat mass (−0.66 kg 95% CI: [−1.00;−0.32]; p < 0.001) compared to the control diet, despite similar energy intake and physical activity levels. This study concludes that while the ketogenic LCHF diet is effective for weight loss, it disproportionately reduces lean mass over fat mass, suggesting the need for concurrent strength training to mitigate muscle loss in women following this diet.
18.	Burén, Jonas, 1984, et al. (author) Evidence of a two-factor structure for Internet Gaming Disorder and Social Media Disorder: Psychometric properties of a new screening instrument for adolescents and adults 2023 In: Journal of Psychopathology and Behavioral Assessment. - 0882-2689 .- 1573-3505. ; 45 Journal article (peer-reviewed)abstract Currently, there is no screening instrument available for assessing both internet gaming disorder (IGD) and social media disorder (SMD). This study aimed to examine the reliability and factor structure of a new screening instrument for adolescents and adults, the Gaming and Social Media Questionnaire (GSMQ-9), and to investigate its association with psychosocial outcomes (i.e., psychosomatic problems, self-concept, and social problems for adults and quality of life for adolescents). Survey data were collected from 995 university students and 626 adolescents. Results showed that a two-factor solution, representing Heavy Involvement and Negative Consequences, had a better model fit compared to a one-factor solution for both IGD and SMD and for both adolescents and adults. The internal consistency was acceptable, and the test-retest reliability was excellent. Negative Consequences were significantly more strongly related to all psychosocial outcomes compared to Heavy Involvement. The proportion of participants meeting the DSM-5 symptom criteria according to self-ratings on the GSMQ-9 was 1.4% (adolescents) and 1.8% (adults) for IGD and 2.6% (adolescents) and 4.0% (adults) for SMD. Conclusively, the GSMQ-9 appears to be a reliable two-factor screening instrument for IGD and SMD among adults and adolescents.
19.	Burén, Jonas, 1984, et al. (author) Gaming and Social Media Addiction in University Students: Sex Differences, Suitability of Symptoms, and Association With Psychosocial Difficulties 2021 In: Frontiers in Psychiatry. - : Frontiers Media SA. - 1664-0640. ; 12 Journal article (peer-reviewed)abstract Background: Previous research has shown that addictions to digital media can have negative impact on psychosocial health. Although Internet Gaming Disorder (IGD) has received most scholarly recognition, the potential negative consequences of Social Media Disorder (SMD) have also been found. However, few studies have assessed the symptoms of these two digital media addictions in the same way, making comparisons difficult. The present study aims to fill this gap by investigating differences and similarities regarding how common the symptoms are, sex differences, the suitability of the symptoms, and their association with psychosocial difficulties. Method: A total of 688 university students (63.2% women, Mean age = 25.98) completed a questionnaire measuring symptoms of IGD and SMD, as well as psychosocial difficulties (i.e., psychosomatic symptoms, low self-concept, and social problems). Results: Results showed that 1.2% of the men and 0.9% of the women met the symptom criteria for IGD (non-significant difference), whereas 3.2% men and 2.8% women met the symptom criteria for SMD (non-significant difference). Dimensional analyses indicated that men had higher IGD scores compared to women, whereas the opposite was found for SMD. Symptoms of heavy involvement in digital media (i.e., Preoccupation, Tolerance, Withdrawal, Unsuccessful attempts to control, and Escape) had high sensitivity, but low positive predictive value (PPV). However, symptoms associated with negative consequences of digital media use (i.e., Loss of interest, Continued excessive use, Deception, and Jeopardizing career/relationships) had low sensitivity, but high PPV. These symptom patterns were similar for IGD and SMD. Meeting the criteria for IGD or SMD as well as being at risk of these disorders were significantly associated with psychosocial difficulties. Symptoms of SMD generally had stronger associations with psychosomatic symptoms compared to symptoms of IGD. Conclusions: We conclude that heavy involvement in digital media seems common among individuals with IGD or SMD, but also among those not meeting the symptom criteria, whereas negative consequences are less common but highly predictive of digital media addictions once present. Further attention to SMD is warranted, as it seems more common than IGD and also seems to be equally or more strongly associated with psychosocial difficulties.
20.	Burén, Jonas, 1972- (author) Glucose and lipid metabolism in insulin resistance : an experimental study in fat cells 2003 Doctoral thesis (other academic/artistic)abstract Type 2 diabetes is usually caused by a combination of pancreatic β-cell failure and insulin resistance in target tissues like liver, muscle and fat. Insulin resistance is characterised by an impaired effect of insulin to reduce hepatic glucose production and to promote glucose uptake in peripheral tissues. The focus of this study was to further elucidate cellular mechanisms for insulin resistance that may be of relevance for type 2 diabetes in humans. We used rat and human adipocytes as an established model of insulin’s target cells. Glucocorticoids, e.g. cortisol, can induce insulin resistance in vivo. In the present study, pretreatment of rat adipocytes in vitro for 24 h with the cortisol analogue dexamethasone produced a downregulation of glucose uptake capacity as well as a marked depletion of cellular insulin receptor substrate 1 (IRS-1) and protein kinase B (PKB), two proteins suggested to play a critical role in the intracellular signal transduction pathway of insulin. The amount of phosphorylated PKB in response to acute insulin treatment was decreased in parallel to total PKB content. The basal rate of lipolysis was enhanced, but insulin’s antilipolytic effect was not consistently altered following dexamethasone pretreatment. Alterations in blood glucose as well as insulin levels may be of great importance for cellular as well as whole-body insulin resistance. High glucose (≥15 mM) for 24 h induced a decrease in glucose uptake capacity in rat adipocytes and IRS-1 content was reduced whereas IRS-2 was increased. Long-term pretreatment with a high insulin concentration downregulated insulin binding capacity and when combined with high glucose, it produced a pronounced reduction of cellular IRS-1 and 2 content together with insensitivity to insulin’s effect to activate PKB and a decrease in glucose uptake capacity. A common denominator for a decrease in glucose uptake capacity in our rat adipocyte studies seems to be a decrease in IRS-1 content. Adipocytes from type 2 diabetes patients are insulin-resistant, but in our work the insulin resistance could be reversed by incubation of the cells at a physiological glucose level for 24 h. Insulin resistance in fresh adipocytes from type 2 diabetes patients was associated with in vivo insulin resistance and glycemic level and with adipocyte cell size and waist-hip ratio (WHR). As a potential mechanism for postprandial dyslipidemia in type 2 diabetes, we examined the nutritional regulation of subcutaneous adipose tissue lipoprotein lipase (LPL) activity. It was upregulated by ~40-50 % after a standardised lipid-enriched meal and this was very similar in type 2 diabetes patients and control subjects, suggesting that the postprandial hypertriglyceridemia found in type 2 diabetes is not explained by an altered nutritional regulation of LPL in subcutaneous fat. In conclusion, the present work provides evidence for novel interactions between glucocorticoids and insulin in the regulation of glucose metabolism that may potentially contribute to the development of insulin resistance. High levels of glucose and insulin produce perturbations in the insulin signalling pathway that may be of relevance for human type 2 diabetes. Cellular insulin resistance may be secondary to the diabetic state in vivo, e.g. via glucotoxicity. This is supported by our finding that insulin resistance in adipocytes from type 2 diabetes patients can be reversed after incubation at a physiological glucose level. Key words: adipocyte, insulin resistance, type 2 diabetes, insulin signalling, glucose uptake, insulin, glucose, dexamethasone, insulin receptor substrate, protein kinase B, GLUT4, lipoprotein lipase.
21.	Burén, Jonas, et al. (author) High glucose and insulin in combination cause insulin receptor substrate-1 and -2 depletion and protein kinase B desensitisation in primary cultured rat adipocytes : possible implications for insulin resistance in type 2 diabetes. 2003 In: European Journal of Endocrinology. - : European Society of Endocrinology. - 0804-4643 .- 1479-683X. ; 148:1, s. 157-67 Journal article (peer-reviewed)abstract OBJECTIVE: The purpose of this study was to investigate the cellular effects of long-term exposure to high insulin and glucose levels on glucose transport and insulin signalling proteins.DESIGN AND METHODS: Rat adipocytes were cultured for 24 h in different glucose concentrations with 10(4) microU/ml of insulin or without insulin. After washing, (125)I-insulin binding, basal and acutely insulin-stimulated d-[(14)C]glucose uptake, and insulin signalling proteins and glucose transporter 4 (GLUT4) were assessed.RESULTS: High glucose (15 and 25 mmol/l) for 24 h induced a decrease in basal and insulin-stimulated glucose uptake compared with control cells incubated in low glucose (5 or 10 mmol/l). Twenty-four hours of insulin treatment decreased insulin binding capacity by approximately 40%, and shifted the dose-response curve for insulin's acute effect on glucose uptake 2- to 3-fold to the right. Twenty-four hours of insulin treatment reduced basal and insulin-stimulated glucose uptake only in the presence of high glucose (by approximately 30-50%). At high glucose, insulin receptor substrate-1 (IRS-1) expression was downregulated by approximately 20-50%, whereas IRS-2 was strongly upregulated by glucose levels of 10 mmol/l or more (by 100-400%). Insulin treatment amplified the suppression of IRS-1 when combined with high glucose and also IRS-2 expression was almost abolished. Twenty-four hours of treatment with high glucose or insulin, alone or in combination, shifted the dose-response curve for insulin's effect to acutely phosphorylate protein kinase B (PKB) to the right. Fifteen mmol/l glucose increased GLUT4 in cellular membranes (by approximately 140%) compared with 5 mmol/l but this was prevented by a high insulin concentration.CONCLUSIONS: Long-term exposure to high glucose per se decreases IRS-1 but increases IRS-2 content in rat adipocytes and it impairs glucose transport capacity. Treatment with high insulin downregulates insulin binding capacity and, when combined with high glucose, it produces a marked depletion of IRS-1 and -2 content together with an impaired sensitivity to insulin stimulation of PKB activity. These mechanisms may potentially contribute to insulin resistance in type 2 diabetes.
22.	Buren, Jonas, et al. (author) Hippocampal 11beta-hydroxysteroid dehydrogenase type 1 messenger ribonucleic acid expression has a diurnal variability that is lost in the obese Zucker rat. 2007 In: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 148:6, s. 2716-22 Journal article (peer-reviewed)
23.	Burén, Jonas, et al. (author) In vitro reversal of hyperglycemia normalizes insulin action in fat cells from type 2 diabetes patients : is cellular insulin resistance caused by glucotoxicity in vivo? 2003 In: Metabolism. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 52:2, s. 239-45 Journal article (peer-reviewed)abstract Chronic hyperglycemia promotes the development of insulin resistance. The aim of this study was to investigate whether cellular insulin resistance is secondary to the diabetic state in human type 2 diabetes. Subcutaneous fat biopsies were taken from 3 age-, sex-, and body mass index (BMI)-matched groups with 10 subjects in each group: type 2 diabetes patients with either good (hemoglobin A(1c) [HbA(1c)] < 7%, G) or poor (HbA(1c) > 7.5%, P) metabolic control and healthy control subjects (C). Insulin action in vitro was studied by measurements of glucose uptake both directly after cell isolation and following a 24-hour incubation at a physiological glucose level (6 mmol/L). The relationship with insulin action in vivo was addressed by employing the euglycemic clamp technique. Freshly isolated fat cells from type 2 diabetes patients with poor metabolic control had approximately 55% lower maximal insulin response (1,000 microU/mL) on glucose uptake (P <.05) compared to C. Cells from P were more insulin-resistant (P <.05) than cells from G at a low (5 microU/mL) but not at a high (1,000 microU/mL) insulin concentration, suggesting insulin insensitivity. However, following 24 hours of incubation at physiological glucose levels, insulin resistance was completely reversed in the diabetes cells and no differences in insulin-stimulated glucose uptake were found among the 3 groups. Insulin sensitivity in vivo assessed with hyperinsulinemic, euglycemic clamp (M-value) was significantly associated with insulin action on glucose uptake in fresh adipocytes in vitro (r = 0.50, P <.01). Fasting blood glucose at the time of biopsy and HbA(1c), but not serum insulin, were negatively correlated to insulin's effect to stimulate glucose uptake in vitro (r = -0.36, P =.064 and r = - 0.41, P <.05, respectively) in all groups taken together. In the in vivo situation, fasting blood glucose, HbA(1c), and serum insulin were all negatively correlated to insulin sensitivity (M-value; r = -0.62, P<.001, r= -0.61, P<.001, and r = -0.56, p <.01, respectively). Cell size, waist-to-hip ration (WHR), and BMI correlated negatively with insulin's effect to stimulate glucose uptake both in vitro (r = -0.55, P <.01, r = -0.54, P <.01, and r = -0.43, P <.05, respectively) and in vivo (r = -0.43, P <.05, r = -0.50, P <.01, and r = -0.36, P <.05, respectively). Multiple regression analyses revealed that adipocyte cell size and WHR independently predicted insulin resistance in vitro. Furthermore, insulin sensitivity in vivo could be predicted by fasting blood glucose and serum insulin levels. We conclude that insulin resistance in fat cells from type 2 diabetes patients is fully reversible following incubation at physiological glucose concentrations. Thus, cellular insulin resistance may be mainly secondary to the hyperglycemic state in vivo.
24.	Burén, Jonas, et al. (author) Insulin action and signalling in fat and muscle from dexamethasone-treated rats 2008 In: Archives of Biochemistry and Biophysics. - : Elsevier BV. - 0003-9861 .- 1096-0384. ; 474:1, s. 91-101 Journal article (peer-reviewed)abstract Glucocorticoids initiate whole body insulin resistance and the aim of the present study was to investigate effects of dexamethasone on protein expression and insulin signalling in muscle and fat tissue. Rats were injected with dexamethasone (1mg/kg/day, i.p.) or placebo for 11 days before insulin sensitivity was evaluated in vitro in soleus and epitrochlearis muscles and in isolated epididymal adipocytes. Dexamethasone treatment reduced insulin-stimulated glucose uptake and glycogen synthesis by 30-70% in epitrochlearis and soleus, and insulin-stimulated glucose uptake by approximately 40% in adipocytes. 8-bromo-cAMP-stimulated lipolysis was approximately 2-fold higher in adipocytes from dexamethasone-treated rats and insulin was less effective to inhibit cAMP-stimulated lipolysis. A main finding was that dexamethasone decreased expression of PKB and insulin-stimulated Ser(473) and Thr(308) phosphorylation in both muscles and adipocytes. Expression of GSK-3 was not influenced by dexamethasone treatment in muscles or adipocytes and insulin-stimulated GSK-3beta Ser(9) phosphorylation was reduced in muscles only. A novel finding was that glycogen synthase (GS) Ser(7) phosphorylation was higher in both muscles from dexamethasone-treated rats. GS expression decreased (by 50%) in adipocytes only. Basal and insulin-stimulated GS Ser(641) and GS Ser(645,649,653,657) phosphorylation was elevated in epitrochlearis and soleus muscles and GS fractional activity was reduced correspondingly. In conclusion, dexamethasone treatment (1) decreases PKB expression and insulin-stimulated phosphorylation in both muscles and adipocytes, and (2) increases GS phosphorylation (reduces GS fractional activity) in muscles and decreases GS expression in adipocytes. We suggest PKB and GS as major targets for dexamethasone-induced insulin resistance.
25.	Burén, Jonas, et al. (author) Is insulin resistance caused by defects in insulin's target cells or by a stressed mind? 2005 In: Diabetes/Metabolism Research Reviews. - : John Wiley & Sons. - 1520-7552 .- 1520-7560. ; 21:6, s. 487-494 Journal article (other academic/artistic)abstract The importance of understanding insulin action is emphasized by the increasing prevalence of insulin resistance in various populations and by the fact that it plays an important pathophysiological role in many common disorders, for example, diabetes, obesity, hypertension and dyslipidemia. The primary factors responsible for the development of insulin resistance are so far unknown, although both genetic and environmental factors are involved. The genetic defects responsible for the common forms of insulin resistance, for example, in type 2 diabetes, are largely unidentified. Some studies from our group as well as by other investigators suggest that cellular insulin resistance is reversible and that it may be secondary to factors in the in vivo environment. These may include insulin-antagonistic action of hormones like catecholamines, glucocorticoids, sex steroids and adipokines as well as dysregulation of autonomic nervous activity and they could contribute to the early development of insulin resistance. Some of these factors can directly impair glucose uptake capacity and this might be due to alterations in key proteins involved in insulin's intracellular signaling pathways. This article briefly summarizes proposed mechanisms behind cellular and whole-body insulin resistance. In particular, we question the role of intrinsic defects in insulin's target cells as primary mechanisms in the development of insulin resistance in type 2 diabetes and we suggest that metabolic and neurohormonal factors instead are the main culprits.
26.	Burén, Jonas, 1984, et al. (author) Prevalence and predictors of sexting among early adolescents in Sweden 2017 In: 18th Conference of the European Association of Developmental Psychology (EADP). Utrecht, The Netherlands: 29 August - 1 september 2017. Conference paper (other academic/artistic)abstract Sexting, here referring to sending nude or sexually explicit images or videos, appears to be fairly common among late adolescents. However, very few studies have focused on sexting among younger adolescents. The purpose of this study was to examine the prevalence of sexting among Swedish high school students, and the links between different psychosocial factors (social support from family and peers, offline- and online peer victimization) and sexting in this age group. In total, 916 adolescents from Swedish high-schools (grade 7 to 9, 13 – 16 years) completed a survey about sexting. The study showed that for both boys and girls it was more common to receive and to send sexts among older high school students (figure 1 and 2). Hierarchical binary logistic regression showed that, for boys, age, social support and online peer victimization emerged as significant predictors of both receiving and sending sexts. For girls, only age and online victimization emerged as a significant predictor of receiving and sending sexts. These predictors remained significant after controlling for age, family income, school satisfaction and subjective well-being in subsequent steps (see Table 1 and 2). In sum, the present study indicates that sexting is quite common also among younger adolescents. For both girls and boys, sexting seems to be increasing with age, and is linked to adverse online experiences with peers. From the present study, it also seems important to direct attention towards the role of social support for boys’ experiences of sexting. The findings will be further discussed from the viewpoint of adolescent development and the current knowledge about adolescent sexting.
27.	Burén, Jonas, et al. (author) Reply to Ravnskov, U. Is High Cholesterol Deleterious? An Alternative Point of View. Comment on “Burén et al. A Ketogenic Low-Carbohydrate High-Fat Diet Increases LDL Cholesterol in Healthy, Young, Normal-Weight Women: A Randomized Controlled Feeding Trial. Nutrients 2021, 13, 814” 2021 In: Nutrients. - : MDPI. - 2072-6643. ; 13:7 Journal article (peer-reviewed)abstract We thank Ravnskov [...]
28.	Burén, Jonas, 1984, et al. (author) Screen time and addictive use of gaming and social media in relation to health outcomes 2023 In: Frontiers in Psychology. - 1664-1078. ; 14 Journal article (peer-reviewed)abstract Introduction: This study examined associations between screen time and addictive use (i.e., heavy involvement and negative consequences) of gaming and social media, and their independent effects on health outcomes. Methods: Survey data were collected from 2,265 participants (mean age = 21.57). Internet Gaming Disorder (IGD) and Social Media Disorder (SMD) were measured with the Gaming and Social Media Questionnaire (GSMQ-9), with separate measures for heavy involvement and negative consequences. Screen time was measured by weekly hours of gaming and social media. Assessed health outcomes were psychological problems, low self-concept, social problems, sleep problems, and sleep time. Results: Screen time and addictive use were significantly associated for both gaming and social media, with associations being stronger for symptoms of heavy involvement compared to symptoms of negative consequences. However, despite significant associations, a substantial proportion of the participants with a high screen time did not meet any or just one symptom of addiction. More importantly, it was primarily negative consequences that had independent effects on health outcomes, except for sleep. High levels of heavy involvement in gaming, were even related to lower, not higher, levels of psychological problems. Conclusion: The present findings study show that screen time is a poor indicator of addictive use of gaming and social media. Given that it was primarily negative consequences of gaming or social media that had effects on health outcomes, our study also emphasizes the need to distinguish between different types of addictive use and to further examine the diagnostic validity of the nine IGD symptom criteria.
29.	Burén, Jonas, 1984 (author) Sexting among adolescents 2018 Licentiate thesis (other academic/artistic)abstract The present thesis aim to examine Swedish adolescents’ experiences with sexting. As adolescents are in the midst of major developmental changes: physical, cognitive, and social ones, and in a period of sexual exploration, understanding of sexting among adolescents is important. Similar to other sexual activities, sexting is heavily influenced by the social context, for example family, peers and social norms. Although scientific research on adolescent sexting has burgeoned in recent years, several questions about adolescents’ sexting experiences remain unanswered, such as who adolescents primarily send sexts to, and what the social norms about sexting is among adolescents and their peers. Studies 1 and 2, included in this thesis, were used to address these issues. Also, with the indication that sexting is a gendered phenomenon, gender was a central theme in this thesis. In Study 1, a total of 1653 adolescents (mean age 14.20) answered a questionnaire. Results showed that, depending on who the sexting partner was, prevalence rates ranged from 4.4% to 16.0% for sending sext, and from 23.5% to 26.8% for receiving sexts. It was most common for participants to send sext to a romantic partner, and the least common was to a stranger. Girls had more negative experiences of sexting, and felt more pressure to send sexts. Importantly, and although boys’ experiences of sexting were more positive than were girls’, a substantial share of boys also reported having negative experiences. Age, puberty, online risk-taking, and peer- and family support, predicted sexting, but different patterns emerged depending on whom the sext was sent to, and depending on gender. In Study 2, 719 answers to an open-ended question focusing on adolescents’ perceptions of peer approval of sexting, were analyzed for content. The content analysis indicated that sexting could be seen as an acceptable activity given that certain circumstances were fulfilled, such as sexting within a romantic relationship or if both parties agree to sext. The adolescents also thought that girls were unfairly treated for sexting, that sexting held certain risks, and that some adolescents may engage in sexting for attention or pleasure. This thesis concluded with a discussion concerning the importance of considering who adolescent sext with, what risks may be perceived by some adolescents, and that sexting is a gendered and complex phenomenon that is heavily influenced by several factors around the adolescent.
30.	Burén, Jonas, 1984 (author) Sexting among adolescents: A gendered online phenomenon, related to individual and social determinants 2020 Doctoral thesis (other academic/artistic)abstract This thesis concerns sexting among Swedish adolescents and adolescent sexual development. Adolescence is a period of major bodily, cognitive, and social changes and of sexual exploration. As many post-millennials have intertwined their lives with digital technologies, this sexual exploration also occurs in the digital context in the form of sexting. Sexting is the sending of nude or semi-nude pictures or video clips online. With sexting being a relatively common phenomenon among adolescents, questions have been raised concerning why adolescents engage in it and with whom, what sexting experiences adolescents have, and how sexting affects adolescent sexual development. Answering these questions may be central to better understanding adolescent sexting and, more importantly, may shed light on the role of sexting in healthy adolescent sexual development. The three constituent studies of this thesis addressed these questions. In Study I, 1653 adolescents (mean age 14.20 years) completed a questionnaire. The results indicated that, depending on whom the adolescent had sexted with, the prevalence rates were 4.4–16.0% for sending sexts and 23.5–26.8% for receiving sexts. It was most common for participants to send sexts to a romantic partner, and the least common to a stranger. Girls were more likely to report negative experiences of sexting than were boys and felt more pressure to send sexts. Developmental factors such as age, perceived pubertal timing, online risk-taking, and peer and family support were all related to sexting, but different relationship patterns emerged depending on gender and to whom the sext was sent. In Study II, a hypothesized model was tested using SEM to examine whether different aspects of body image were related to sexting. The study showed that sexting was more common among adolescents who perceived appearance to be important for their self-image and in their social context (i.e., dysfunctional appearance beliefs). How much one monitors and views one’s body as an object of others’ desire (i.e., self-objectification) was also related to sexting with a stranger among boys. In Study III, 808 answers to an openended question were qualitatively analyzed for content, to examine the social norms that operate in the adolescents’ peer groups. Among peers, sexting was seen as an acceptable activity based on certain conditions, for example, that it occurs within a trusting relationship and that there is mutual agreement between the sexting partners. It was not seen as an accepted practice if, for example, the partner was someone unknown. In the peer group, it was also perceived that girls were unfairly treated when engaging in sexting, that sexting entailed certain risks, and that some adolescents may engage in sexting for attention or pleasure. The results of the three studies were discussed in relation to the overarching aims of the thesis. More specifically, sexting was assumed to be related to several psychosocial factors within and outside the adolescent. It was also concluded that it is important to consider whom the adolescents’ sext with and that although sexting may play an important role in adolescents’ sexual exploration and expression, it may also entail certain risks of harm. Sexting can be understood as one sexual behavior among others that may fit into adolescent sexual development.
31.	Burén, Jonas, 1984, et al. (author) Sexting among adolescents: A nuanced and gendered online challenge for young people 2018 In: Computers in Human Behavior. - : Elsevier BV. - 0747-5632. ; 85, s. 210-217 Journal article (peer-reviewed)abstract This study examined adolescents' sexting experiences, with an emphasis on the prevalence of sending and receiving sexts from romantic partners, friends/peers, online friends, and strangers. We also examined the quality of sexting experiences and individual and psychosocial factors associated with sending sexts. In total, 1653 Swedish adolescents aged 12 to 16 (M age=14.16) completed a questionnaire. We found that 20–32% reported having received sexts and 4–16% having sent sexts. These rates typically differed depending on who the participants received sext from or sent sext to. Girls experienced more pressure to send sexts, and had more negative sexting experiences. Multiple logistic regressions showed significant relationships between online risk-taking, age, pubertal timing, family income, family and friend support, and sending sexts. The strength of these relationships differed by gender and by who the sext was sent to. This study highlights the importance of viewing adolescents’ sexting as a complex and gendered online phenomenon.
32.	Burén, Jonas, 1984, et al. (author) What do peers think about sexting? Adolescents' views of the norms guiding sexting behavior 2022 In: Journal of Adolescent Research. - : SAGE Publications. - 0743-5584 .- 1552-6895. ; 37:2 Journal article (peer-reviewed)abstract This study examined the content of injunctive peer norms (i.e., perceived peer approval) of sexting among Swedish adolescents. Written answers from 808 adolescents (Mage = 14.22) to an open-ended question about peers’ views of sexting were analyzed qualitatively using content analysis. Eight categories were distinguished for when and why sexting is acceptable or not in the peer group. A substantial share of adolescents believed their peers approve of sexting, especially if sexting occurs within trusted relationships and when all parties have consented. A large share of adolescents described that peers were non-accepting of sexting, emphasizing that it can be spread to others. The participants also suggested that sexting is seen as a gendered phenomenon surrounded by sexual double standards, with girls at more risk of negative consequences. Some participants emphasized the peer view that adolescents sext to seek attention, and some emphasized that sexting is viewed as an enjoyable activity. Several of these categories’ likelihood to be mentioned was related to the adolescents’ age, gender, and prior experience of sexting. We concluded that adolescents might have a hard time navigating the social context of sexting, given the conflicting and gendered messages from peers.
33.	Ericsson, Madelene, et al. (author) Försämrad hjärtfunktion efter fyra veckors intag av lågkolhydrat/högfettkost hos möss : Kan vi lära av translationell forskning? 2017 In: Svensk kardiologi. - 1400-5816. ; :1, s. 33-35 Journal article (pop. science, debate, etc.)
34.	Eriksson, Jan, et al. (author) Postprandial regulation of blood lipids and adipose tissue lipoprotein lipase in type 2 diabetes patients and healthy control subjects 2003 In: Atherosclerosis. - : Elsevier. - 0021-9150 .- 1879-1484. ; 166:2, s. 359-367 Journal article (peer-reviewed)abstract Background/aim: In type 2 diabetes and other insulin-resistant conditions, postprandial hypertriglyceridaemia is an important metabolic perturbation. To further elucidate alterations in the clearance of triglyceride-rich lipoproteins in type 2 diabetes we focused on the nutritional regulation of adipose tissue lipoprotein lipase (LPL).Subjects and methods: Eight subjects with type 2 diabetes and eight age-, sex- and body mass index (BMI)-matched control subjects underwent subcutaneous abdominal adipose tissue biopsies in the fasting state and 3.5 h following a standardized lipid-enriched meal. LPL activity and mass were measured in adipose tissue and also in plasma after an intravenous injection of heparin.Results: Postprandial, but not fasting, triglycerides were significantly higher in the diabetic subjects than in the control subjects (3.0±0.4 vs 2.0±0.2 mmol/l, P=0.028). Adipose tissue LPL activity was increased following the meal test by ∼35–55% (P=0.021 and 0.004, respectively). There was no significant difference between the groups in this respect. The specific enzyme activity of LPL was not altered in the postprandial state. Fasting and postprandial adipose tissue LPL activity as well as post-heparin plasma LPL activity tended to be lower among the diabetes patients (NS). There was a significant and independent inverse association between insulin resistance (homeostasis model assessment insulin resistance (HOMA-IR) index) vs post-heparin plasma LPL activity and postprandial triglyceride levels, respectively. Adipose tissue LPL activity was related to insulin action in vitro on adipocyte glucose transport, but not to HOMA-IR.Conclusion: Following food intake adipose tissue LPL activity is enhanced to a similar degree in patients with type 2 diabetes and in healthy control subjects matched for BMI, age and gender. If LPL dysregulation is involved in the postprandial hypertriglyceridaemia found in type 2 diabetes, it should occur in tissues other than subcutaneous fat.
35.	Evans, Juliet, et al. (author) Depot- and ethnic-specific differences in the relationship between adipose tissue inflammation and insulin sensitivity 2011 In: Clinical Endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 74:1, s. 51-59 Journal article (peer-reviewed)abstract Objective It is unclear whether there are differences in inflammatory gene expression between abdominal and gluteal subcutaneous adipose tissue (SAT), and between black and white women. We therefore tested the hypotheses that SAT inflammatory gene expression is greater in the abdominal compared to the gluteal depot, and SAT inflammatory gene expression is associated with differential insulin sensitivity (S(I) ) in black and white women. Design and methods S(I) (frequently sampled intravenous glucose tolerance test) and abdominal SAT and gluteal SAT gene expression levels of 13 inflammatory genes were measured in normal-weight (BMI 18-25 kg/m(2) ) and obese (BMI >30 kg/m(2) ) black (n = 30) and white (n = 26) South African women. Results Black women had higher abdominal and gluteal SAT expression of CCL2, CD68, TNF-α and CSF-1 compared to white women (P < 0·01). Multivariate analysis showed that inflammatory gene expression in the white women explained 56·8% of the variance in S(I) (P < 0·005), compared to 20·9% in black women (P = 0·30). Gluteal SAT had lower expression of adiponectin, but higher expression of inflammatory cytokines, macrophage markers and leptin than abdominal SAT depots (P < 0·05). Conclusions Black South African women had higher inflammatory gene expression levels than white women; however, the relationship between AT inflammation and S(I) was stronger in white compared to black women. Further research is required to explore other factors affecting S(I) in black populations. Contrary to our original hypothesis, gluteal SAT had a greater inflammatory gene expression profile than abdominal SAT depots. The protective nature of gluteo-femoral fat therefore requires further investigation.
36.	Goding, Therese, et al. (author) Bättre kostvanor nyckel till ökade prestationer 2011 In: Svensk Idrottsmedicin. - : Södertälje Svensk idrottsmedicinsk förening. - 1103-7652. ; :2, s. 26-29 Journal article (pop. science, debate, etc.)
37.	Hou, Miao, et al. (author) Neonatal overfeeding induced by small litter rearing causes altered glucocorticoid metabolism in rats 2011 In: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 6:11, s. e25726- Journal article (peer-reviewed)abstract Elevated glucocorticoid (GC) activity may be involved in the development of the metabolic syndrome. Tissue GC exposure is determined by the tissue-specific GC-activating enzyme 11 beta-hydroxysteriod dehydrogenase type 1 (11 beta-HSD1) and the GC-inactivating enzyme 5 alpha-reductase type 1 (5 alpha R1), as well as 5 beta-reductase (5 beta R). Our aim was to study the effects of neonatal overfeeding induced by small litter rearing on the expression of GC-regulating enzymes in adipose tissue and/or liver and on obesity-related metabolic disturbances during development. Male Sprague-Dawley rat pup litters were adjusted to litter sizes of three (small litters, SL) or ten (normal litters, NL) on postnatal day 3 and then given standard chow from postnatal week 3 onward (W3). Small litter rearing induced obesity, hyperinsulinemia, and higher circulating corticosterone in adults. 11 beta-HSD1 expression and enzyme activity in retroperitoneal, but not in epididymal, adipose tissue increased with postnatal time and peaked at W5/W6 in both groups before declining. From W8, 11 beta-HSD1 expression and enzyme activity levels in retroperitoneal fat persisted at significantly higher levels in SL compared to NL rats. Hepatic 11 beta-HSD1 enzyme activity in SL rats was elevated from W3 to W16 compared to NL rats. Hepatic 5 alpha R1 and 5 beta R expression was higher in SL compared to NL rats after weaning until W6, whereupon expression decreased in the SL rats and remained similar to that in NL rats. In conclusion, small litter rearing in rats induced peripheral tissue-specific alterations in 11 beta-HSD1 expression and activity and 5 alpha R1 and 5 beta R expression during puberty, which could contribute to elevated tissue-specific GC exposure and aggravate the development of metabolic dysregulation in adults.
38.	Hou, Miao, et al. (author) The effects of dietary fatty acid composition in the post-sucking period on metabolic alterations in adulthood : can omega 3 polyunsaturated fatty acids prevent adverse programming outcomes? 2012 In: Journal of Endocrinology. - 0022-0795 .- 1479-6805. ; 215:1, s. 119-127 Journal article (peer-reviewed)abstract Early life nutrition is important in the regulation of metabolism in adulthood. We studied the effects of different fatty acid composition diets on adiposity measures, glucose tolerance, and peripheral glucocorticoid (GC) metabolism in overfed neonatal rats. Rat litters were adjusted to a litter size of three (small litters (SLs)) or ten (normal litters (NLs)) on postnatal day 3 to induce overfeeding or normal feeding respectively. After weaning, SL and NL rats were fed a omega 6 polyunsaturated fatty acid (PUFA) diet (14% calories as fat, soybean oil) or high-saturated fatty acid (high-fat; 31% calories as fat, lard) diet until postnatal week 16 respectively. SL rats were also divided into the third group fed a omega 3 PUFA diet (14% calories as fat, fish oil). A high-fat diet induced earlier and/or more pronounced weight gain, hyperphagia, glucose intolerance, and hyperlipidemia in SL rats compared with NL rats. In addition, a high-fat diet increased 11 beta-hsd1 (Hsd11b1) mRNA expression and activity in the retroperitoneal adipose tissue of both litter groups compared with standard chow counterparts, whereas high-fat feeding increased hepatic 11 beta-hsd1 mRNA expression and activity only in SL rats. SL and a high-fat diet exhibited significant interactions in both retroperitoneal adipose tissue and hepatic 11 beta-HSD1 activity. Dietary omega 3 PUFA offered protection against glucose intolerance and elevated GC exposure in the retroperitoneal adipose tissue and liver of SL rats. Taken together, the results suggest that dietary fatty acid composition in the post-sucking period may interact with neonatal feeding and codetermine metabolic alterations in adulthood. Journal of Endocrinology (2012) 215, 119-127
39.	Ji, Chenlin, et al. (author) Postnatal overfeeding promotes early onset and exaggeration of high-fat diet-induced nonalcoholic fatty liver disease through disordered hepatic lipid metabolism in rats 2014 In: Journal of Nutritional Biochemistry. - : Elsevier. - 0955-2863 .- 1873-4847. ; 25:11, s. 1108-1116 Journal article (peer-reviewed)abstract Exposure to overnutrition in critical or sensitive developmental periods may increase the risk of developing obesity and metabolic syndrome in adults. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome, but the relationship among postnatal nutrition, lipid metabolism, and NAFLD progression during development remains poorly understood. Here we investigated in a rat model whether postnatal overfeeding increases susceptibility to NAFLD in response to a high-fat diet. Litters from Sprague-Dawley dams were culled to three (small litters) or ten (normal litters) pups and then weaned onto a standard or high-fat diet at postnatal day 21 to generate normal-litter, small-litter, normal-litter/high-fat, and small-litter/high-fat groups. At age 16 weeks, the small-litter and both high-fat groups showed obesity, dyslipidemia, and insulin resistance. Hepatic disorders appeared earlier in the small-litter/high-fat rats with greater liver mass gain and higher hepatic triglycerides and steatosis score versus normal-litter/high-fat rats. Hepatic acetyl-CoA carboxylase activity and mRNA expression were increased in small-litter rats and aggravated in small-litter/high-fat rats but not in normal-litter/high-fat rats. The high expression in small-litter/high-fat rats coincided with high sterol regulatory element-binding protein-1c mRNA and protein expression. However, mRNA expression of enzymes involved in hepatic fatty acid oxidation (carnitine palmitoyltransferase 1) and output (microsomal triglyceride transfer protein) was decreased under a high-fat diet regardless of litter size. In conclusion, overfeeding related to small-litter rearing during lactation contributes to the NAFLD phenotype when combined with a high-fat diet, possibly through up-regulated hepatic lipogenesis. (C) 2014 Elsevier Inc. All rights reserved.
40.	Lindholm, Åsa Maria, 1958-, et al. (author) Adipose tissue inflammation in polycystic ovary syndrome (PCOS) Other publication (other academic/artistic)abstract Context: Previous studies have indicated that peripheral circulating markers of inflammation are elevated in women with polycystic ovary syndrome (PCOS). Thus far, no studies concerning adipose tissue expression of inflammatory markers have been conducted in PCOS patients. Objectives: The aim of the study was to investigate if PCOS patients display increased adipose tissue expression of inflammatory markers. Design and Settings: Cross-sectional study at three out-patient gynecologic departments. Participants and Approach: Ten lean PCOS patients, 20 overweight PCOS patients, and 20 overweight controls underwent subcutaneous fat biopsies and blood samples. Main Outcome Measures: Adipose tissue gene expression of inflammatory markers, circulating markers of inflammation, and obesity-related metabolic disturbances. Results: Overweight PCOS patients had higher relative amounts of adipose tissue CCL2, CCR2, TNF-a, IL-18, CD14 and CD163 mRNA expression compared to lean PCOS women. There were no differences between overweight PCOS patients and overweight control subjects in this respect. Within the PCOS group, markers of adipose tissue inflammation correlated significantly with obesity-related metabolic disturbances, but when data were adjusted for age and BMI most correlations were lost. Conclusion: Overweight, rather than the PCOS diagnosis per se, appears to be the main explanatory variable for elevated adipose tissue inflammation in PCOS patients. Our findings suggest that lean PCOS patients carry less risk for metabolic complications later on in life.
41.	Lindholm, Åsa, et al. (author) No difference in markers of adipose tissue inflammation between overweight women with polycystic ovary syndrome and weight-matched controls 2011 In: Human Reproduction. - : Oxford University Press (OUP). - 0268-1161 .- 1460-2350. ; 26:6, s. 1478-1485 Journal article (peer-reviewed)abstract Background: Previous studies have indicated that peripheral circulating markers of inflammation are elevated in women with polycystic ovary syndrome (PCOS), but thus far no studies concerning markers of inflammation in adipose tissue have been published. The aim of the study was to investigate whether patients with PCOS display increased expression of inflammatory markers in adipose tissue. Methods: Twenty overweight patients with PCOS, 10 lean patients with PCOS and 20 overweight controls had subcutaneous fat biopsies and blood samples taken. Adipose tissue levels of mRNA of inflammatory markers were determined by use of real-time PCR. Results: Overweight patients with PCOS had higher relative adipose tissue chemokine ligand 2 (P < 0.01), and its cognate receptor (P < 0.05), tumour necrosis factor-alpha (P < 0.001), interleukin (IL)-10 (P < 0.001) and IL-18 (P < 0.001) and the monocyte/ macrophage markers CD14 (P < 0.01) and CD163 (P < 0.01) mRNA levels compared with lean women with PCOS. There were no differences between overweight patients with PCOS and overweight control subjects in this respect. Within the PCOS group, markers of adipose tissue inflammation correlated significantly with obesity-related metabolic disturbances, but when data were adjusted for age and BMI, most correlations were lost. Conclusions: Overweight, rather than the PCOS diagnosis per se, appears to be the main explanatory variable for elevated adipose tissue inflammation in patients with PCOS.
42.	Lindmark, Stina, et al. (author) Insulin resistance, endocrine function and adipokines in type 2 diabetes patients at different glycaemic levels : potential impact for glucotoxicity in vivo 2006 In: Clinical Endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 65:3, s. 301-309 Journal article (peer-reviewed)abstract Objective To evaluate the interplay between hyperglycaemia, insulin resistance, hormones and adipokines in patients with type 2 diabetes mellitus (T2DM). Design and methods Ten patients with T2DM with good glycaemic control (G), 10 with poor control (P) and 10 nondiabetic control subjects (C) were matched for sex (M/F 6/4), age and body mass index. A hyperinsulinaemic, euglycaemic clamp was performed and cytokines and endocrine functions, including cortisol axis activity were assessed. Results Patients with diabetes were more insulin resistant than group C, and group P exhibited the highest degree of insulin resistance ( P = 0·01, P vs C). Tumour necrosis factor (TNF)-alpha levels were elevated in patients with diabetes ( P = 0·05) and group P had the highest levels of fasting serum cortisol ( P = 0·05), nonesterified fatty acids (NEFA; P = 0·06) and C-reactive protein (CRP; P = 0·01). Adiponectin levels were lower in the P group. In partial correlation analyses, significant associations were found: glycaemic level (HbA1c) with insulin resistance, TNF-alpha, CRP and basal and ACTH-stimulated cortisol levels, insulin resistance with plasma NEFA, TNF-alpha and stimulated cortisol levels. Conclusion Poor glycaemic control in patients with T2DM was associated with insulin resistance and with elevated TNF-alpha, CRP and basal as well as stimulated cortisol levels. Inflammatory mediators, e.g. TNF-alpha, may contribute to insulin resistance in hyperglycaemic patients with T2DM and this might be a partial explanation for glucotoxicity.
43.	Lunde, Carolina, 1979, et al. (author) Sexting experiences and motivations among adolescents with ADHD and ASD 2023 In: Computers in Human Behavior. - : Elsevier BV. - 0747-5632. ; 140 Journal article (peer-reviewed)abstract Sexting (i.e., to send and receive self-produced sexual materials) has become a common element in adolescents’ socio-sexual exploration. Although often harmless, sexting also involves the risk of abuse, and potentially more so for some adolescents than for others. Adolescents with attention deficit disorder (ADHD) and/or autism spectrum disorder (ASD) have been pointed out as potentially more vulnerable online, yet research to support or reject these concerns is sparse. Focusing on sending sexts, this study compares sexting rates, sexting experiences, and sexting motivations of Swedish adolescents with ADHD and/or ASD to adolescents without these diagnoses. In all, 1063 adolescents (aged 15 to 19), 164 of whom self-reported ADHD and/or ASD, completed a survey about their sexting experiences. The results revealed both differences and similarities between groups. Adolescents with ADHD sexted more and reported more pressure to sext. No group differences were noted in terms of reporting positive or negative experiences. Sexting motivations were also similar between groups, although sexting for aggravated reasons was more common among adolescents with ADHD and/or ASD. Our findings suggest that adolescents with ADHD and ASD mainly use sexting for sexual gratification and exploration, but also report experiences and motivations that may indicate increased vulnerability in relation to sexting.
44.	Lundgren, Magdalena, et al. (author) Glucocorticoids down-regulate glucose uptake capacity and insulin-signaling proteins in omental but not subcutaneous human adipocytes. 2004 In: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 89:6, s. 2989-2997 Journal article (peer-reviewed)
45.	Lundgren, Magdalena, 1973- (author) Interplay between hormones, nutrients and adipose depots in the regulation of insulin sensitivity : an experimental study in rat and human adipocytes 2006 Doctoral thesis (other academic/artistic)abstract Obesity and specifically central obesity is related to insulin resistance, type 2 diabetes and other components of the so-called metabolic syndrome. The aim of this study was to elucidate the interplay between hormones, nutrients and adipose depots in normal and insulin-resistant fat cell metabolism.High levels of free fatty acids (FFAs) induce insulin resistance in muscle and liver in vivo. In the present study, rat adipocytes were treated with high physiological levels of oleic or palmitic acid in vitro for 4-24 h. This treatment had no effect on basal or insulin-stimulated glucose uptake capacity in these cells, neither did it affect the levels of the insulin signalling proteins; insulin receptor substrate (IRS)-1 or –2, phosphatidylinositol 3-kinase (PI3-K), protein kinase B (PKB) or glucose transporter (GLUT) 4, or the regulation of lipolysis rate.Visceral adiposity is considered to be more harmful than peripheral adiposity with respect to metabolic and cardiovascular complications. In adipose biopsies from subjects undergoing abdominal surgery, we found that glucose uptake capacity was elevated in omental as compared to subcutaneous adipocytes. The sensitivity (EC50) or maximum relative response to insulin, measured as % of basal, did however not differ between the depots. In women, subcutaneous adipocytes displayed a higher lipolysis rate following cAMP-stimulation than omental adipocytes, whereas there was a tendency towards the opposite in adipocytes from men. No differences were found between depots or sexes in the ability of insulin to inhibit lipolysis or in the levels of the lipolysis regulating proteins, i.e. protein kinase A (PKA), hormone sensitive lipase (HSL) and perilipin.Glucocorticoids, e.g. cortisol, exert pronounced insulin-antagonistic effects and are associated with redistribution of fat from peripheral to central fat depots in humans. Treatment of human subcutaneous and omental adipocytes in vitro, with the cortisol analogue dexamethasone, resulted in a dose dependent down-regulation of basal and insulin-stimulated glucose uptake capacity in omental, but not in subcutaneous cells. Concomitantly, the levels of IRS-1 and PKB were decreased only in omental adipocytes after dexamethasone treatment. The relative effect of insulin to stimulate glucose uptake was however not altered by dexamethasone treatment. The cAMP-stimulated lipolysis rate was elevated by dexamethasone treatment in cells from the subcutaneous depot in women and tended to be elevated in omental cells from men. No alterations however, were seen in the levels of the assessed lipolysis regulating proteins.Subcutaneous as well as omental fat cell size correlated negatively to insulin action in subcutaneous fat cells in vitro after adjusting for age, sex and body fat parameters in non-diabetic, but not in type 2 diabetic, subjects. Large subcutaneous fat cell size was strongly related to plasma leptin levels in non-diabetic and in type 2 diabetic subjects.We conclude that 1) adipocytes seem to be less vulnerable to elevated levels of fatty acids than muscle and liver cells, 2) the interactions between glucocorticoids and insulin in the regulation of glucose uptake differ between adipose depots, 3) depot specific hormonal lipolysis regulation differs between sexes and 4) fat cell size is related to insulin action in subcutaneous fat cells and to circulating levels of leptin.
46.	Lundgren, Magdalena, et al. (author) Sex- and depot-specific lipolysis regulation in human adipocytes : interplay between adrenergic stimulation and glucocorticoids 2008 In: Hormone and Metabolic Research. - Stuttgart, New York : Georg Thieme Verlag KG. - 0018-5043 .- 1439-4286. ; 40, s. 854-860 Journal article (peer-reviewed)abstract The purpose of this investigation was to explore interactions between adrenergic stimulation, glucocorticoids, and insulin on the lipolytic rate in isolated human adipocytes from subcutaneous and omental fat depots, and to address possible sex diff erences. Fat biopsies were obtained from 48 nondiabetic subjects undergoing elective abdominal surgery. Lipolysis rate was measured as glycerol release from isolated cells and proteins involved in lipolysis regulation were assessed by immunoblots. Fasting blood samples were obtained and metabolic and infl ammatory variables were analyzed. In women, the rate of 8-bromo-cAMP- and isoprenaline-stimulated lipolysis was ~ 2- and 1.5-fold higher, respectively, in subcutaneous compared to omental adipocytes, whereas there was no diff erence between the two depots in men. Dexamethasone treatment increased the ability of 8-bromo-cAMP to stimulate lipolysis in the subcutaneous depot in women, but had no consistent eff ects in fat cells from men. Protein kinase A, Perilipin A, and hormone sensitive lipase content in adipocytes was not aff ected by adipose depot, sex, or glucocorticoid treatment. In conclusion, catecholamine and glucocorticoid regulation of lipolysis in isolatedhuman adipocytes diff ers between adipose tissue depots and also between sexes. These findings may be of relevance for the interaction between endogenous stress hormones and adipose tissue function in visceral adiposity and the metabolic syndrome.
47.	Lundgren, Magdalena, et al. (author) Sex differences in depot-specific lipolysis regulation in human adipocytes : interplay between adrenergic stimulation, glucocorticoids and insulin Other publication (pop. science, debate, etc.)
48.	Nilsson, Jessica, et al. (author) A low-carbohydrate high-fat diet decreases lean mass and impairs cardiac function in pair-fed female C57BL/6J mice 2016 In: Nutrition & Metabolism. - : BioMed Central (BMC). - 1743-7075. ; 13 Journal article (peer-reviewed)abstract BACKGROUND: Excess body fat is a major health issue and a risk factor for the development of numerous chronic diseases. Low-carbohydrate diets like the Atkins Diet are popular for rapid weight loss, but the long-term consequences remain the subject of debate. The Scandinavian low-carbohydrate high-fat (LCHF) diet, which has been popular in Scandinavian countries for about a decade, has very low carbohydrate content (~5 E %) but is rich in fat and includes a high proportion of saturated fatty acids. Here we investigated the metabolic and physiological consequences of a diet with a macronutrient composition similar to the Scandinavian LCHF diet and its effects on the organs, tissues, and metabolism of weight stable mice.METHODS: Female C57BL/6J mice were iso-energetically pair-fed for 4 weeks with standard chow or a LCHF diet. We measured body composition using echo MRI and the aerobic capacity before and after 2 and 4 weeks on diet. Cardiac function was assessed by echocardiography before and after 4 weeks on diet. The metabolic rate was measured by indirect calorimetry the fourth week of the diet. Mice were sacrificed after 4 weeks and the organ weight, triglyceride levels, and blood chemistry were analyzed, and the expression of key ketogenic, metabolic, hormonal, and inflammation genes were measured in the heart, liver, and adipose tissue depots of the mice using real-time PCR.RESULTS: The increase in body weight of mice fed a LCHF diet was similar to that in controls. However, while control mice maintained their body composition throughout the study, LCHF mice gained fat mass at the expense of lean mass after 2 weeks. The LCHF diet increased cardiac triglyceride content, impaired cardiac function, and reduced aerobic capacity. It also induced pronounced alterations in gene expression and substrate metabolism, indicating a unique metabolic state.CONCLUSIONS: Pair-fed mice eating LCHF increased their percentage of body fat at the expense of lean mass already after 2 weeks, and after 4 weeks the function of the heart deteriorated. These findings highlight the urgent need to investigate the effects of a LCHF diet on health parameters in humans.
49.	Renström, Frida, et al. (author) Factors in serum from type 2 diabetes patients can cause cellular insulin resistance 2009 In: Horm Metab Res. - : Georg Thieme Verlag KG. - 1439-4286 .- 1439-4286 .- 0018-5043. ; 41:10, s. 767-72 Journal article (peer-reviewed)abstract This pilot study was aimed to investigate whether there are humoral factors in serum from type 2 diabetic subjects that, in addition to glucose, insulin and free fatty acids are able to induce or contribute to peripheral insulin resistance with respect to glucose transport. Isolated subcutaneous adipocytes from 11 type 2 diabetic subjects and 10 nondiabetic controls were incubated for 24-h in medium supplemented with 25 % serum from a control or a type 2 diabetic donor, in the presence of a low (5 mM) or a high (15 mM) glucose concentration, respectively. After the incubation period glucose uptake capacity was assessed. Serum from type 2 diabetic donors, compared to serum from controls, significantly reduced the maximal insulin eff ect to stimulate glucose uptake (approximately 40 %, p < 0.05) in adipocytes from control subjects, independent of surrounding glucose concentrations. Glucose uptake capacity in adipocytes isolated from type 2 diabetic subjects was similar regardless of culture condition. No significant alterations were found in cellular content of key proteins in the insulin signaling cascade (insulin receptor substrate-1 and -2, and glucose transporter 4) that could explain the impaired insulin-stimulated glucose transport in control adipocytes incubated with serum from type 2 diabetic donors. The present findings indicate the presence of biomolecules in the circulation of type 2 diabetic subjects, apart from glucose, insulin, and free fatty acids with the ability to induce peripheral insulin resistance. This further implies that even though normoglycemia is achieved other circulating factors can still negatively aff ect insulin sensitivity in type 2 diabetic patients.
50.	Renström, Frida, et al. (author) Insulin receptor substrates-1 and -2 are both depleted but via different mechanisms after down-regulation of glucose transport in rat adipocytes. 2005 In: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 146:7, s. 3044-3051 Journal article (peer-reviewed)abstract Alterations in muscle and adipose tissue insulin receptor substrate (IRS)-1 and IRS-2 are associated with, and commonly believed to contribute to, development of insulin resistance. In this study, we investigated the mechanisms behind previously observed reductions in IRS levels due to high concentrations of glucose and insulin and their significance in the impairment of glucose uptake capacity in primary rat adipocytes. Semiquantitative RT-PCR analysis showed that insulin (104 μU/ml) alone or in combination with glucose (15 mm) markedly suppressed IRS-2 gene expression, whereas IRS-1 mRNA was unaffected by the culture conditions. The negative effect of a high glucose/high insulin setting on IRS-1 protein level was still exerted when protein synthesis was inhibited with cycloheximide. Impairment of glucose uptake capacity after treatment with high glucose and insulin was most pronounced after 3 h, whereas IRS-1 and IRS-2 protein levels were unaffected up to 6 h but were reduced after 16 h. Moreover, impaired glucose uptake capacity could only partially be reversed by subsequent incubation at physiological conditions. These novel results suggest that: 1) in a high glucose/high insulin setting depletion of IRS-1 and IRS-2 protein, respectively, occurs via different mechanisms, and IRS-2 gene expression is suppressed, whereas IRS-1 depletion is due to posttranslational mechanisms; 2) IRS-1 and IRS-2 protein depletion is a secondary event in the development of insulin resistance in this model of hyperglycemia/hyperinsulinemia; and 3) depletion of cellular IRS in adipose tissue may be a consequence rather than a cause of insulin resistance and hyperinsulinemia in type 2 diabetes.

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