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- Cavalera, Michele, et al.
(författare)
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Rose hip supplementation increases energy expenditure and induces browning of white adipose tissue
- 2016
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Ingår i: Nutrition & Metabolism. - : Springer Science and Business Media LLC. - 1743-7075. ; 13:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Overweight and obesity are widespread chronic disorders defined as excessive fat accumulation, and are major risk factors for several chronic diseases including type 2 diabetes, coronary heart disease, high blood pressure and fatty liver. Changes in lifestyle such as increased physical activity and a healthy diet can be crucial tools for treating obesity. Intake of rose hip, the fruit of several plants belonging to the Rosaceae family, has been shown to reduce body fat mass and prevent body weight gain. Thus, the aim of the study was to elucidate potential mechanisms through which rose hip inhibit diet-induced obesity. Methods: C57BL/6 J mice were fed a high fat diet with (RH) or without (CTR) rose hip supplementation for three months. In vivo indirect calorimetry was monitored, as well as gene expression and protein levels of different adipose depots. Results: Although no differences in energy intake were found compared to the CTR group, RH prevented body weight gain and lowered blood glucose, insulin and cholesterol levels. Indirect calorimetry showed that RH-fed mice have significantly higher EE during the dark phase, despite comparable voluntary activity. Moreover, when challenged with treadmill running, RH-fed mice exhibited higher metabolic rate. Therefore, we hypothesized that RH could stimulate the brown adipose tissue (BAT) thermogenic capacity or may induce browning of the white adipose tissue (WAT). Compared to the CTR group, gene expression and protein levels of some brown and "brite"markers, together with genes able to promote brown adipocyte differentiation and thermogenesis (such as ucp1, tbx15, bmp7, and cidea), as well as phosphorylation of AMPK, was increased in WAT (but not in BAT) of RH-fed mice. Conclusions: Taken together these results indicate that dietary rose hip prevents body weight gain by increasing whole body EE and inducing browning of WAT. Thus, it has potential therapeutic implication for treatment of obesity and related metabolic disorders.
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- Cen, Jing, et al.
(författare)
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Fatty acids stimulate insulin secretion from human pancreatic islets at fasting glucose concentrations via mitochondria-dependent and -independent mechanisms
- 2016
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Ingår i: Nutrition & Metabolism. - : Springer Science and Business Media LLC. - 1743-7075. ; 13
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Tidskriftsartikel (refereegranskat)abstract
- Background: Free fatty acids (FFAs) acutely stimulate insulin secretion from pancreatic islets. Conflicting results have been presented regarding this effect at non-stimulatory glucose concentration, however. The aim of our study was to investigate how long-chain FFAs affect insulin secretion from isolated human pancreatic islets in the presence of physiologically fasting glucose concentrations and to explore the contribution of mitochondria to the effects on secretion. Methods: Insulin secretion from human pancreatic islets was measured from short-term static incubation or perfusion system at fasting glucose concentration (5.5 mM) with or without 4 different FFAs (palmitate, palmitoleate, stearate, and oleate). The contribution of mitochondrial metabolism to the effects of fatty acid-stimulated insulin secretion was explored. Results: The average increase in insulin secretion, measured from statically incubated and dynamically perifused human islets, was about 2-fold for saturated free fatty acids (SFAs) (palmitate and stearate) and 3-fold for mono-unsaturated free fatty acids (MUFAs) (palmitoleate and oleate) compared with 5.5 mmol/l glucose alone. Accordingly, MUFAs induced 50 % and SFAs 20 % higher levels of oxygen consumption compared with islets exposed to 5.5 mmol/l glucose alone. The effect was due to increased glycolysis. When glucose was omitted from the medium, addition of the FFAs did not affect oxygen consumption. However, the FFAs still stimulated insulin secretion from the islets although secretion was more than halved. The mitochondria-independent action was via fatty acid metabolism and FFAR1/GPR40 signaling. Conclusions: The findings suggest that long-chain FFAs acutely induce insulin secretion from human islets at physiologically fasting glucose concentrations, with MUFAs being more potent than SFAs, and that this effect is associated with increased glycolytic flux and mitochondrial respiration.
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- Dimova, Lidiya G., et al.
(författare)
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High- cholesterol diet does not alter gut microbiota composition in mice
- 2017
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Ingår i: Nutrition & Metabolism. - : BIOMED CENTRAL LTD. - 1743-7075. ; 14
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Western diet containing both saturated fat and cholesterol impairs cardio- metabolic health partly by modulating diversity and function of the microbiota. While diet containing only high fat has comparable effects, it is unclear how diets only enriched in cholesterol impact the microbiota. Therefore, we aimed to characterize the response of host and microbiota to a high cholesterol ( HC) diet in mice susceptible to cardio- metabolic disease. Methods: LDLR knockout mice received either 1.25% HC or no cholesterol containing control diet ( NC) for 12 weeks before characterizing host cholesterol metabolism and intestinal microbiota composition ( next generation sequencing). Results: HC diet substantially increased plasma ( 1.6- fold) and liver cholesterol levels ( 21- fold), biliary cholesterol secretion ( 4.5- fold) and fecal neutral sterol excretion ( 68- fold, each p < 0.001) but not fecal bile acid excretion. Interestingly, despite the profound changes in intestinal cholesterol homeostasis no differences in microbial composition between control and HC- fed mice were detected. In both groups the main phyla were Bacteroidetes ( 55%), Firmicutes ( 27%) and Verrucomicrobia ( 14%). Conclusion: Our results demonstrate that in mice HC diet alone does not alter the microbiota composition despite inducing substantial adaptive changes in whole body cholesterol homeostasis. The impact of Western diet on intestinal microbiota thus appears to be mediated exclusively by its high fat content.
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- Forsum, Elisabet, et al.
(författare)
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MET-values of standardised activities in relation to body fat: studies in pregnant and non-pregnant women
- 2018
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Ingår i: Nutrition & Metabolism. - : BIOMED CENTRAL LTD. - 1743-7075. ; 15
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Tidskriftsartikel (refereegranskat)abstract
- Background: Physical activity is associated with health in women. Published MET-values (MET: metabolic equivalent of task) may assess physical activity and energy expenditure but tend to be too low for subjects with a high total body fat (TBF) content and therefore inappropriate for many contemporary women. The MET-value for an activity is the energy expenditure of a subject performing this activity divided by his/her resting energy expenditure, often assumed to be 4.2 kJ/kg/h. Relationships between TBF and MET have been little studied although overweight and obesity is common in women. Available data indicate that MET-values decrease during pregnancy but more studies in pregnant contemporary women are needed. Subjects and methods: Using indirect calorimetry we measured energy expenditure and assessed MET-values in women, 22 non-pregnant (BMI: 18-34) and 22 in gestational week 32 (non-pregnant BMI: 18-32) when resting, sitting, cycling (30 and 60 watts), walking (3.2 and 5.6 km/h) and running (8 km/h). Relationships between TBF and MET-values were investigated and used to predict modified MET-values. The potential of such values to improve calculations of total energy expenditure of women was investigated. Results: The resting energy expenditure was below 4.2 kJ/kg/h in both groups of women. Women in gestational week 32 had a higher resting energy metabolism (p amp;lt; 0.001) and 7-15% lower MET-values (p amp;lt; 0.05) than non-pregnant women. MET-values of all activities were correlated with TBF (p amp;lt; 0.05) in non-pregnant women and modified MET-values improved estimates of total energy expenditure in such women. In pregnant women, correlations (p amp;lt;= 0.03) between TBF and MET were found for running (8 km/h) and for walking at 5.6 km/h. Conclusions: Our results are relevant when attempts are made to modify the MET-system in contemporary pregnant and non-pregnant women. MET-values were decreased in gestational week 32, mainly due to an increased resting energy metabolism and studies describing how body composition affects the one MET-value (i.e. the resting energy metabolism in kJ/kg/h) during pregnancy are warranted. Studies of how pregnancy and TBF affect MET-values of high intensity activities are also needed. Corrections based on TBF may have a potential to improve the MET-system in non-pregnant women.
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- Li, M. Z., et al.
(författare)
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Decreased secretion of adiponectin through its intracellular accumulation in adipose tissue during tobacco smoke exposure
- 2015
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Ingår i: Nutrition & Metabolism. - : Springer Science and Business Media LLC. - 1743-7075. ; 12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Cigarette smoking is associated with an increased risk of type 2 diabetes mellitus (T2DM). Smokers exhibit low circulating levels of total adiponectin (ADPN) and high-molecular-weight (HMW) ADPN multimers. Blood concentrations of HMW ADPN multimers closely correlate with insulin sensitivity for handling glucose. How tobacco smoke exposure lowers blood levels of ADPN, however, has not been investigated. In the current study, we examined the effects of tobacco smoke exposure in vitro and in vivo on the intracellular and extracellular distribution of ADPN and its HMW multimers, as well as potential mechanisms. Findings: We found that exposure of cultured adipocytes to tobacco smoke extract (TSE) suppressed total ADPN secretion, and TSE administration to mice lowered their plasma ADPN concentrations. Surprisingly, TSE caused intracellular accumulation of HMW ADPN in cultured adipocytes and in the adipose tissue of wild-type mice, while preferentially decreasing HMW ADPN in culture medium and in plasma. Importantly, we found that TSE up-regulated the ADPN retention chaperone ERp44, which colocalized with ADPN in the endoplasmic reticulum. In addition, TSE down-regulated DsbA-L, a factor for ADPN secretion. Conclusions: Tobacco smoke exposure traps HMW ADPN intracellularly, thereby blocking its secretion. Our results provide a novel mechanism for hypoadiponectinemia, and may help to explain the increased risk of T2DM in smokers.
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- Marungruang, Nittaya, et al.
(författare)
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Heat-treated high-fat diet modifies gut microbiota and metabolic markers in apoe-/- mice
- 2016
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Ingår i: Nutrition & Metabolism. - : Springer Science and Business Media LLC. - 1743-7075. ; 13, s. 22-22
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: High-fat diet has been known to have adverse effects on metabolic markers, as well as the gut microbiota. However, the effect of heat processing of high-fat diet, which leads to formations of advanced glycation end products (AGEs) has not been clearly distinguished from the effect of unheated fat. This study compared the effect of high-fat diet with heat-treated high-fat diet on adiposity, atherosclerosis and gut microbiota composition in the caecum of apoe (-/-) mice.METHOD: Male apoe (-/-) mice were fed either low-fat (LF) control diet, high-fat (40 E% saturated fat, HF) control diet, or heat-treated high-fat (200 °C for 10 min, HT) diet, for 8 weeks. The plasma samples were used in the analysis of Nε-carboxy-methyl-lysine (CML) and Nε-carboxy-ethyl-lysine (CEL). The heart samples were analysed for atherosclerotic plaques, and the DNA from caecum was extracted and analysed for microbiota composition using 16S rRNA gene sequencing on a Miseq instrument. Additionally, the functions of microbial communities were also predicted based on the bacterial 16S rRNA gene sequence using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt).RESULTS: Here we found that HT modifies gut microbiota composition and host adiposity. Prediction of bacterial gene functions based on 16S rRNA gene sequence revealed that HF increased bacterial genera enriched in lipid metabolism genes, while HT did not. Plasma CML and CEL increased 1.7 and 2.5 times, respectively, in mice fed HT as compared to mice fed HF. Despite lower adiposity, mice fed HT maintained atherosclerosis and displayed enlarged spleens.CONCLUSIONS: The results suggested that heat processing of high-fat diet modifies the substrates reaching the lower gut of apoe (-/-) mice, resulting in different effects on gut microbiota composition. AGEs seem to maintain the effect on atherosclerosis, despite lower adiposity, and causing enlarged spleens, which possibly reflect elevated levels of inflammation in the body.
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- Melnik, Bodo C., et al.
(författare)
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Milk miRNAs : Simple nutrients or systemic functional regulators?
- 2016
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Ingår i: Nutrition & Metabolism. - : Springer Science and Business Media LLC. - 1743-7075. ; 13:1
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Tidskriftsartikel (refereegranskat)abstract
- Milk is rich in miRNAs that appear to play important roles in the postnatal development of all mammals. Currently, two competing hypotheses exist: the functional hypothesis, which proposes that milk miRNAs are transferred to the offspring and exert physiological regulatory functions, and the nutritional hypothesis, which suggests that these molecules do not reach the systemic circulation of the milk recipient, but merely provide nutrition without conferring active regulatory signals to the offspring. The functional hypothesis is based on indirect evidence and requires further investigation. The nutritional hypothesis is primarily based on three mouse models, which are inherently problematic: 1) miRNA-375 KO mice, 2) miRNA-200c/141 KO mice, and 3) transgenic mice presenting high levels of miRNA-30b in milk. This article presents circumstantial evidence that these mouse models may all be inappropriate to study the physiological traffic of milk miRNAs to the newborn mammal, and calls for new studies using more relevant mouse models or human milk to address the fate and role of milk miRNAs in the offspring and the adult consumer of cow's milk.
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| 10. |
- Nilsson, Jessica, et al.
(författare)
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A low-carbohydrate high-fat diet decreases lean mass and impairs cardiac function in pair-fed female C57BL/6J mice
- 2016
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Ingår i: Nutrition & Metabolism. - : BioMed Central (BMC). - 1743-7075. ; 13
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Tidskriftsartikel (refereegranskat)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.
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