| 1. |
- Benedict, Christian, et al.
(författare)
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Acute Sleep Deprivation Enhances the Brain's Response to Hedonic Food Stimuli : An fMRI Study
- 2012
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 97:3, s. E443-447
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Tidskriftsartikel (refereegranskat)abstract
- Context:There is growing recognition that a large number of individuals living in Western society are chronically sleep deprived. Sleep deprivation is associated with an increase in food consumption and appetite. However, the brain regions that are most susceptible to sleep deprivation-induced changes when processing food stimuli are unknown.Objective:Our objective was to examine brain activation after sleep and sleep deprivation in response to images of food.Intervention:Twelve normal-weight male subjects were examined on two sessions in a counterbalanced fashion: after one night of total sleep deprivation and one night of sleep. On the morning after either total sleep deprivation or sleep, neural activation was measured by functional magnetic resonance imaging in a block design alternating between high- and low-calorie food items. Hunger ratings and morning fasting plasma glucose concentrations were assessed before the scan, as were appetite ratings in response to food images after the scan.Main Outcome Measures:Compared with sleep, total sleep deprivation was associated with an increased activation in the right anterior cingulate cortex in response to food images, independent of calorie content and prescan hunger ratings. Relative to the postsleep condition, in the total sleep deprivation condition, the activation in the anterior cingulate cortex evoked by foods correlated positively with postscan subjective appetite ratings. Self-reported hunger after the nocturnal vigil was enhanced, but importantly, no change in fasting plasma glucose concentration was found.Conclusions:These results provide evidence that acute sleep loss enhances hedonic stimulus processing in the brain underlying the drive to consume food, independent of plasma glucose levels. These findings highlight a potentially important mechanism contributing to the growing levels of obesity in Western society.
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| 2. |
- Benedict, Christian, et al.
(författare)
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Acute sleep deprivation reduces energy expenditure in healthy men
- 2011
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 93:6, s. 1229-1236
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundEpidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown.ObjectiveWe examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans.DesignAccording to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session.ResultsIn comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by approximate to 5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected.ConclusionOur findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.
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| 3. |
- Benedict, Christian, et al.
(författare)
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Diurnal Rhythm of Circulating Nicotinamide Phosphoribosyltransferase (Nampt/Visfatin/PBEF) : Impact of Sleep Loss and Relation to Glucose Metabolism
- 2012
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 97:2, s. E218-E222
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Tidskriftsartikel (refereegranskat)abstract
- Context Animal studies indicate that nicotinamide phosphoribosyltransferase [Nampt/visfatin/pre-B-cell colony-enhancing factor (PBEF)] contributes to the circadian fine-tuning of metabolic turnover. However, it is unknown whether circulating Nampt concentrations, which are elevated in type 2 diabetes and obesity, display a diurnal rhythm in humans.Objective Our objective was to examine the 24-h profile of serum Nampt in humans under conditions of sleep and sleep deprivation and relate the Nampt pattern to morning postprandial glucose metabolism.InterventionFourteen healthy men participated in two 24-h sessions starting at 1800 h, including either regular 8-h-night sleep or continuous wakefulness. Serum Nampt and leptin were measured in 1.5- to 3-h intervals. In the morning, plasma glucose and serum insulin responses to standardized breakfast intake were determined.Main Outcome Measures Under regular sleep-wake conditions, Nampt levels displayed a pronounced diurnal rhythm, peaking during early afternoon (P < 0.001) that was inverse to leptin profiles peaking in the early night. When subjects stayed awake, the Nampt rhythm was preserved but phase advanced by about 2 h (P < 0.05). Two-hour postprandial plasma glucose concentrations were elevated after sleep loss (P < 0.05), whereas serum insulin was not affected. The relative glucose increase due to sleep loss displayed a positive association with the magnitude of the Nampt phase shift (r = 0.54; P < 0.05).ConclusionsSerum Nampt concentrations follow a diurnal rhythm, peaking in the afternoon. Sleep loss induces a Nampt rhythm phase shift that is positively related to the impairment of postprandial glucose metabolism due to sleep deprivation, suggesting a regulatory impact of Nampt rhythmicity on glucose homeostasis.
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| 4. |
- Benedict, Christian, et al.
(författare)
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Intranasal insulin as a therapeutic option in the treatment of cognitive impairments
- 2011
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Ingår i: Experimental Gerontology. - : Elsevier BV. - 0531-5565 .- 1873-6815. ; 46:2-3, s. 112-115
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Tidskriftsartikel (refereegranskat)abstract
- The brain is a major target of circulating insulin. Enhancing central nervous insulin action has been shown to improve memory functions in animals as well as in humans, benefitting in particular hippocampus-dependent (declarative) memory. As Alzheimer's disease (AD) is associated with reduced central nervous insulin signaling and attenuated permeation of blood-borne insulin across the blood-brain-barrier, the cognitive decline in AD patients may at least in part be derived from impaired brain insulin signaling. Thus, therapeutic strategies to overcome central nervous system insulin deficiency and resistance might be an attractive option in the treatment of cognitive impairments like AD. Insulin can be effectively delivered directly to the brain via the intranasal route that enables the hormone to bypass the blood-brain barrier and modulate central nervous functions. This review summarizes a series of studies demonstrating beneficial effects of intranasal insulin on memory functions both in healthy humans and in patients with cognitive impairments such as AD. These experiments in humans consistently indicate that enhancing brain insulin signaling by intranasal administration of the hormone improves hippocampus-dependent memory in the absence of adverse side effects. Considering that insulin also acts as a neuroprotective signal, up-regulating brain insulin levels by intranasal insulin administration appears to be a promising approach in the treatment and prevention of central nervous system insulin deficiency and resistance as found in AD.
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| 5. |
- Benedict, Christian, et al.
(författare)
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Intranasal Insulin Enhances Postprandial Thermogenesis and Lowers Postprandial Serum Insulin Levels in Healthy Men
- 2011
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Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 60:1, s. 114-118
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE Animal studies indicate a prominent role of brain insulin signaling in the regulation of peripheral energy metabolism. We determined the effect of intranasal insulin, which directly targets the brain, on glucose metabolism and energy expenditure in humans.RESEARCH DESIGN AND METHODSIn a double-blind, placebo-controlled, balanced within-subject comparison, 19 healthy normal-weight men (18-26 years old) were intranasally administered 160 IU human insulin after an overnight fast. Energy expenditure assessed via indirect calorimetry and blood concentrations of glucose, insulin, C-peptide, and free fatty acids (FFAs) were measured before and after insulin administration and the subsequent consumption of a high-calorie liquid meal of 900 kcal.RESULTSIntranasal insulin, compared with placebo, increased postprandial energy expenditure, i.e., diet-induced thermogenesis, and decreased postprandial concentrations of circulating insulin and C-peptide, whereas postprandial plasma glucose concentrations did not differ from placebo values. Intranasal insulin also induced a transient decrease in prandial serum FFA levels.CONCLUSIONSEnhancing brain insulin signaling by means of intranasal insulin administration enhances the acute thermoregulatory and glucoregulatory response to food intake, suggesting that central nervous insulin contributes to the control of whole-body energy homeostasis in humans.
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| 6. |
- Chapman, Colin D, et al.
(författare)
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Intranasal Treatment of Central Nervous System Dysfunction in Humans
- 2013
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Ingår i: Pharmaceutical research. - : Springer Science and Business Media LLC. - 0724-8741 .- 1573-904X. ; 30:10, s. 2475-2484
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Forskningsöversikt (refereegranskat)abstract
- One of the most challenging problems facing modern medicine is how to deliver a given drug to a specific target at the exclusion of other regions. For example, a variety of compounds have beneficial effects within the central nervous system (CNS), but unwanted side effects in the periphery. For such compounds, traditional oral or intravenous drug delivery fails to provide benefit without cost. However, intranasal delivery is emerging as a noninvasive option for delivering drugs to the CNS with minimal peripheral exposure. Additionally, this method facilitates the delivery of large and/or charged therapeutics, which fail to effectively cross the blood-brain barrier (BBB). Thus, for a variety of growth factors, hormones, neuropeptides and therapeutics including insulin, oxytocin, orexin, and even stem cells, intranasal delivery is emerging as an efficient method of administration, and represents a promising therapeutic strategy for the treatment of diseases with CNS involvement, such as obesity, Alzheimer's disease, Parkinson's disease, Huntington's disease, depression, anxiety, autism spectrum disorders, seizures, drug addiction, eating disorders, and stroke.
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| 7. |
- Feld, Gordon B, et al.
(författare)
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Central Nervous Insulin Signaling in Sleep-Associated Memory Formation and Neuroendocrine Regulation
- 2016
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Ingår i: Neuropsychopharmacology. - : Springer Science and Business Media LLC. - 0893-133X .- 1740-634X. ; 41:6, s. 1540-1550
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Tidskriftsartikel (refereegranskat)abstract
- The neurochemical underpinnings of sleep's contribution to the establishment and maintenance of memory traces are largely unexplored. Considering that intranasal insulin administration to the CNS improves memory functions in healthy and memory-impaired humans, we tested whether brain insulin signaling and sleep interact to enhance memory consolidation in healthy participants. We investigated the effect of intranasal insulin on sleep-associated neurophysiological and neuroendocrine parameters and memory consolidation in 16 men and 16 women (aged 18-30 years), who learned a declarative word-pair task and a procedural finger sequence tapping task in the evening before intranasal insulin (160 IU) or placebo administration and 8 h of nocturnal sleep. On the subsequent evening, they learned interfering word-pairs and a new finger sequence before retrieving the original memories. Insulin increased growth hormone concentrations in the first night-half and EEG delta power during the second 90 min of non-rapid-eye-movement sleep. Insulin treatment impaired the acquisition of new contents in both the declarative and procedural memory systems on the next day, whereas retrieval of original memories was unchanged. Results indicate that sleep-associated memory consolidation is not a primary mediator of insulin's acute memory-improving effect, but that the peptide acts on mechanisms that diminish the subsequent encoding of novel information. Thus, by inhibiting processes of active forgetting during sleep, central nervous insulin might reduce the interfering influence of encoding new information.
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| 8. |
- Freiherr, Jessica, et al.
(författare)
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Intranasal Insulin as a Treatment for Alzheimer's Disease : A Review of Basic Research and Clinical Evidence
- 2013
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Ingår i: CNS Drugs. - : Springer Science and Business Media LLC. - 1172-7047 .- 1179-1934. ; 27:7, s. 505-514
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Forskningsöversikt (refereegranskat)abstract
- Research in animals and humans has associated Alzheimer's disease (AD) with decreased cerebrospinal fluid levels of insulin in combination with decreased insulin sensitivity (insulin resistance) in the brain. This phenomenon is accompanied by attenuated receptor expression of insulin and insulin-like growth factor, enhanced serine phosphorylation of insulin receptor substrate-1, and impaired transport of insulin across the blood-brain barrier. Moreover, clinical trials have demonstrated that intranasal insulin improves both memory performance and metabolic integrity of the brain in patients suffering from AD or its prodrome, mild cognitive impairment. These results, in conjunction with the finding that insulin mitigates hippocampal synapse vulnerability to beta amyloid, a peptide thought to be causative in the development of AD, provide a strong rationale for hypothesizing that pharmacological strategies bolstering brain insulin signaling, such as intranasal administration of insulin, could have significant potential in the treatment and prevention of AD. With this view in mind, the review at hand will present molecular mechanisms potentially underlying the memory-enhancing and neuroprotective effects of intranasal insulin. Then, we will discuss the results of intranasal insulin studies that have demonstrated that enhancing brain insulin signaling improves memory and learning processes in both cognitively healthy and impaired humans. Finally, we will provide an overview of neuroimaging studies indicating that disturbances in insulin metabolism-such as insulin resistance in obesity, type 2 diabetes and AD-and altered brain responses to insulin are linked to decreased cerebral volume and especially to hippocampal atrophy.
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| 9. |
- Haugg, Amelie, et al.
(författare)
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Predictors of real-time fMRI neurofeedback performance and improvement - A machine learning mega-analysis.
- 2021
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Ingår i: NeuroImage. - : Elsevier. - 1053-8119 .- 1095-9572. ; 237
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Tidskriftsartikel (refereegranskat)abstract
- Real-time fMRI neurofeedback is an increasingly popular neuroimaging technique that allows an individual to gain control over his/her own brain signals, which can lead to improvements in behavior in healthy participants as well as to improvements of clinical symptoms in patient populations. However, a considerably large ratio of participants undergoing neurofeedback training do not learn to control their own brain signals and, consequently, do not benefit from neurofeedback interventions, which limits clinical efficacy of neurofeedback interventions. As neurofeedback success varies between studies and participants, it is important to identify factors that might influence neurofeedback success. Here, for the first time, we employed a big data machine learning approach to investigate the influence of 20 different design-specific (e.g. activity vs. connectivity feedback), region of interest-specific (e.g. cortical vs. subcortical) and subject-specific factors (e.g. age) on neurofeedback performance and improvement in 608 participants from 28 independent experiments. With a classification accuracy of 60% (considerably different from chance level), we identified two factors that significantly influenced neurofeedback performance: Both the inclusion of a pre-training no-feedback run before neurofeedback training and neurofeedback training of patients as compared to healthy participants were associated with better neurofeedback performance. The positive effect of pre-training no-feedback runs on neurofeedback performance might be due to the familiarization of participants with the neurofeedback setup and the mental imagery task before neurofeedback training runs. Better performance of patients as compared to healthy participants might be driven by higher motivation of patients, higher ranges for the regulation of dysfunctional brain signals, or a more extensive piloting of clinical experimental paradigms. Due to the large heterogeneity of our dataset, these findings likely generalize across neurofeedback studies, thus providing guidance for designing more efficient neurofeedback studies specifically for improving clinical neurofeedback-based interventions. To facilitate the development of data-driven recommendations for specific design details and subpopulations the field would benefit from stronger engagement in open science research practices and data sharing.
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| 10. |
- Krug, Rosemarie, et al.
(författare)
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Comparable Sensitivity of Postmenopausal and Young Women to the Effects of Intranasal Insulin on Food Intake and Working Memory
- 2010
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 95:12, s. E468-E472
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Tidskriftsartikel (refereegranskat)abstract
- ContextWe have previously shown that enhancing brain insulin signaling by intranasal administration of a single dose of the hormone acutely reduces food intake in young men but not women, whereas its improving effects on spatial and working memory are restricted to young women.ObjectiveAgainst the background of animal studies suggesting that low estrogen concentrations are a prerequisite for the anorexigenic impact of central nervous insulin, we extended our foregoing study by assessing intranasal insulin effects in postmenopausal women with comparatively low estrogen concentrations, expecting them to be more sensitive than young women to the anorexigenic effects of the hormone.Design, Setting, Participants, and InterventionIn a within-subject, double-blind comparison performed at the University of Lubeck, 14 healthy postmenopausal women (body mass index, 23.71 +/- 0.6 kg/m(2); age, 57.61 +/- 1.14 yr) were intranasally administered 160 IU regular human insulin or vehicle.Main Outcome MeasuresSubjects performed a working memory task (digit span) and a hippocampus-dependent visuospatial memory task. Subsequently, free-choice food intake from an ad libitum breakfast buffet was measured.ResultsContrary to expectations, results in postmenopausal women mirrored those found in young women(22.44 +/- 0.63 yr), i.e. insulin administration did not affect food intake (P > 0.46), but did enhance performance in the prefrontal cortex-dependent working memory task (P < 0.05).ConclusionsLow estrogen levels as present in postmenopausal women do not modulate the effects of intranasal insulin in females, suggesting that in humans as opposed to rats, estrogen signaling does not critically alter central nervous system sensitivity to the effects of insulin on energy homeostasis and cognition.Intranasal insulin has comparable effects in postmenopausal and young women, indicating that estrogen does not critically alter central nervous system insulin sensitivity in women.
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| 11. |
- Pitsillos, Tryfonas, et al.
(författare)
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Association Between Objectively Assessed Sleep and Depressive Symptoms During Pregnancy and Post-partum
- 2022
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Ingår i: Frontiers in Global Women's Health. - : Frontiers Media S.A.. - 2673-5059. ; 2
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Sleep problems are common in pregnancy but many studies have relied only on self-reported sleep measures. We studied the association between objectively measured sleep and peripartum depressive symptoms in pregnant women.Material and Methods: Sleep was assessed using Actiwatch accelerometers in a sample of 163 pregnant women in the late first (weeks 11-15) or early second trimester (weeks 16-19). Depressive symptoms were assessed in gestational weeks 17, 32 and at 6 weeks post-partum using the Edinburgh Postnatal Depression Scale (EPDS). Multiple linear regression and logistic regression analyses, adjusting for age, BMI, pre-pregnancy smoking, ongoing mental health problems, trimester and season of sleep assessment were carried out to test the association between sleep and depression. Sleep was measured by total sleep time and sleep efficiency, whereas depression was indicated by depressive symptoms and depression caseness. Results are presented as unstandardized beta (B) coefficients or adjusted odds ratios (AOR) and 95% confidence intervals (CI).Results: Total sleep time ranged from 3 to 9 h (mean 7.1, SD 0.9) and average sleep efficiency was 83% (SD 6.0). Women with the shortest total sleep time, i.e., in the lowest quartile (<6.66 h), reported higher depressive symptoms during pregnancy (week 17, B = 2.13, 95% CI 0.30-3.96; week 32, B = 1.70, 95% CI 0.03-3.37) but not post-partum. Their probability to screen positive for depression in gestational week 17 was increased more than 3-fold (AOR = 3.46, 95% CI 1.07-11.51) but unchanged with regards to gestational week 32 or 6 weeks post-partum. Sleep efficiency was not associated with depressive symptoms at any stage of pregnancy or post-partum.Discussion: In one of the few studies to use objective sleep measures to date, mental health of pregnant women appeared to be affected by shortened sleep, with total sleep time being negatively associated with depressive symptoms in the early second and third trimester. This finding highlights the relevance of identifying and treating sleep impairments in pregnant women early during antenatal care to reduce the risk of concomitant depression.
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| 12. |
- Ritze, Yvonne, et al.
(författare)
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Metabolic and Cognitive Outcomes of Subchronic Once-Daily Intranasal Insulin Administration in Healthy Men
- 2018
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Ingår i: Frontiers in Endocrinology. - : FRONTIERS MEDIA SA. - 1664-2392. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Insulin acts in the brain to limit food intake and improve memory function. We have previously shown that 8 weeks of intranasal insulin delivered in four daily doses of 40 IU decrease body weight and enhance word list recall. In the present study, we investigated the effect on body composition, endocrine parameters, and memory performance of 8 weeks of once-daily administration of 160 IU in healthy men. We assumed that intranasal insulin administered before nocturnal sleep, a period of relative metabolic inactivity that moreover benefits memory formation, would be superior to insulin delivery in the morning and placebo administration. After a 2-week baseline period, healthy male normal-weight subjects (mean age, 27.1 +/- 0.9 years) received either placebo, 160 IU intranasal insulin in the morning, or 160 IU in the evening (n = 12 per group) for 8 consecutive weeks. Throughout the experiment, we measured body weight and body composition as well as circulating concentrations of glucose, insulin, adrenocorticotropin, cortisol, growth hormone, insulin-like growth-factor 1, adiponectin, and leptin. Declarative and procedural memory function was repeatedly assessed by means of, respectively, word list recall and word-stem priming. We found that neither morning nor evening insulin compared to placebo administration induced discernible changes in body weight and body composition. Delayed recall of words showed slight improvements by insulin administration in the evening, and serum cortisol concentrations were reduced after 2 weeks of insulin administration in the morning compared to the other groups. Results indicate that catabolic long-term effects of central nervous insulin delivery necessitate repetitive, presumably pre-meal delivery schedules. The observed memory improvements, although generally weaker than previously found effects, suggest that sleep after intranasal insulin administration may support its beneficial cognitive impact.
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| 13. |
- Schmid, M, et al.
(författare)
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Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men
- 2009
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 90:6, s. 1476-1482
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Tidskriftsartikel (refereegranskat)abstract
- Background: Short sleep duration is correlated with an increased risk of developing obesity and cardiovascular disease, but the mechanisms behind this relation are largely unknown.Objective: We aimed to test the hypothesis that acute sleep loss decreases physical activity while increasing food intake, thereby shifting 2 crucial behavioral components of energy homeostasis toward weight gain.Design: In 15 healthy, normal-weight men, spontaneous physical activity was registered by accelerometry during the entire experiment, and food intake as well as relevant hormones were assessed during a 15-h daytime period after 2 nights of regular sleep (bed time: 2245-0700) and after 2 nights of restricted sleep (bed time: 0245-0700). Experiments were performed in a crossover design.Results: Sleep restriction significantly decreased physical activity during the daytime spent under free-living conditions after the first night of sleep manipulation (P = 0.008). Also, intensities of physical activity were shifted toward lower levels, with less time spent with intense activities (P = 0.046). Total energy intake, feelings of hunger, and appetite as well as ghrelin and leptin concentrations during day 2 remained unaffected by acute sleep restriction.Conclusions: In contrast to our expectation, short-term sleep loss neither increased food intake nor affected concentrations of the hunger-regulating hormones leptin and ghrelin. However, the observed decrease in daytime physical activity may point to another potentially important behavioral mechanism for the health-impairing influence of sleep loss.
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| 14. |
- Thienel, Matthias, et al.
(författare)
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Intranasal insulin decreases circulating cortisol concentrations during early sleep in elderly humans
- 2017
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Ingår i: Neurobiology of Aging. - : Elsevier BV. - 0197-4580 .- 1558-1497. ; 54, s. 170-174
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Tidskriftsartikel (refereegranskat)abstract
- Aging is associated with increases in hypothalamic-pituitary-adrenal (HPA) axis activity that can predispose to metabolic and cognitive impairments. We investigated in elderly and young subjects whether intranasal insulin administration to the human brain reduces early-sleep nadir concentrations of adrenocorticotropin and cortisol, that is, indicators of baseline HPA axis activity. In within-subject comparisons, intranasal insulin (160 IU) or placebo was administered to 14 elderly (mean age 70.0 years) and 30 young (23.6 years) healthy subjects before bedtime. Sleep was polysomno-graphically assessed and blood samples were repeatedly collected. Elderly compared with young participants displayed increased early-sleep cortisol concentrations (p < 0.04) and reductions in slow wave and REM sleep (p < 0.001). Insulin administration reduced cortisol levels between 2300 hours and 0020 hours in the elderly (p = 0.03) but not young participants (p = 0.56; p = 0.003 for interaction). Findings indicate that central nervous insulin acts as an inhibitory signal in basal HPA axis activity regulation and suggest that intranasal insulin may normalize sleep-associated stress axis activity in older age.
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