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ABSTRACT: Sleep and endocrine function are known to be closely related, but studies on the effect of moderate sleep loss on endocrine axes are still sparse. We examined the influence of partial sleep restriction for 2 days on the secretory activity of the thyrotropic axis. Fifteen healthy, normal-weight men were tested in a balanced, cross-over study. Serum concentrations of thyrotrophin (TSH), free triiodothyronine (fT3) and free thyroxine (fT4) were monitored at 1-h intervals during a 15-h daytime period (08:00-23:00 h) following two nights of restricted sleep (bedtime 02:45-07:00 h) and two nights of regular sleep (bedtime 22:45-07:00 h), respectively. Serum concentrations of fT3 (P < 0.026) and fT4 (P = 0.089) were higher after sleep restriction than regular sleep, with a subsequent blunting of TSH concentrations in the evening hours of the sleep restriction condition (P = 0.008). These results indicate profound alterations in the secretory activity of the thyrotropic axis after 2 days of sleep restriction to ~4 h, suggesting that acute partial sleep loss impacts endocrine homeostasis, with potential consequences for health and wellbeing.
Journal of Sleep Research 04/2013; 22(2):166-9. · 3.16 Impact Factor
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ABSTRACT: Besides the well-characterized effects of brain insulin and leptin in regulating food intake, insulin and leptin signaling to the central nervous system modulates a variety of metabolic processes, such as glucose and lipid homeostasis, as well as energy expenditure. This review summarizes the current literature on the contribution of central nervous insulin and leptin action to metabolic control in animals and humans. Potential therapeutic options based on the direct delivery of these peptides to the brain by, for example, intranasal administration, are discussed.
Endocrinology and metabolism clinics of North America 03/2013; 42(1):109-25. · 3.56 Impact Factor
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ABSTRACT: Background:Obesity and arterial hypertension are tightly connected. Obese individuals show significant elevation of vasoconstrictory muscle sympathetic nerve activity (MSNA). Obesity-related hyperleptinemia might play a key role in mediating these effects. Leptin is synthesized in proportion to body fat mass and activates SNA in animal models. In humans, however, direct evidence linking hyperleptinemia to sympathetic activation has not yet been established. In the present study, we characterize the effects of acute hyperleptinemia on microneurographically recorded SNA in humans.Methods:In a balanced, double-blind crossover design, 12 healthy normal-weight males received an iv bolus of leptin or placebo. MSNA (bursts per minute) was continuously recorded using a microneurographic technique. Ten-minute periods were analyzed at resting periods before (t(-100)) and at 20 (t(20)), 60 (t(60)), and 140 (t(140)) minutes after substance administration. Blood pressure and heart rate (HR) were recorded simultaneously.Results:Baseline values of MSNA, blood pressure, and HR were comparable in both conditions (MSNA: t(-100), 24.3 ± 1.6 vs 22.7 ± 1.7, not significant). After application of leptin, MSNA showed a significant increase (t(20), 31.0 ± 1.9 vs. 24.9 ± 1.8, P = .05) that persisted until the end of the experiment (t(60), P = .008; t(140), P = .004). There were no significant changes in blood pressure and HR.Conclusions:Acute experimental hyperleptinemia has significant central nervous excitatory effects on vasoconstrictory sympathetic outflow as measured by MSNA in healthy men. These results suggest that leptin acts as an important mediator linking obesity to elevated MSNA and potentially to the development of hypertension.
The Journal of clinical endocrinology and metabolism 02/2013; · 6.50 Impact Factor
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ABSTRACT: Total sleep deprivation (TSD) exerts strong modulatory effects on the secretory activity of endocrine systems that might be related to TSD-induced challenges of cerebral glucose metabolism. Here, we investigate whether TSD affects the course of male pituitary-gonadal and pituitary-thyroid axis related hormones during a subsequent 240-min hypoglycemic clamp. Ten healthy men were tested on 2 different conditions, TSD and 7-hour regular sleep. Circulating concentrations of total testosterone, prolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT4) were measured during baseline and a subsequent hypoglycemic clamp taking place in the morning. Basal, i.e. at 07∶00 am measured, concentrations of total testosterone (P = 0.05) and PRL (P<0.01) were lower while the values of TSH (P = 0.02), fT3 (P = 0.08), and fT4 (P = 0.04) were higher after TSD as compared to regular sleep. During the subsequent hypoglycemic clamp (all measurements from baseline to the end of the clamp analyzed) total testosterone concentrations in the regular sleep (P<0.01) but not in the TSD condition (P = 0.61) decreased, while PRL levels increased (P = 0.05) irrespectively of the experimental condition (P = 0.31). TSH concentrations decreased during hypoglycemia (P<0.01), with this decrease being more pronounced after TSD (P = 0.04). However, at the end of the hypoglycemic clamp concentrations all of the above mentioned hormones did not differ between the two sleep conditions. Our data indicate a profound influence of TSD on male pituitary-gonadal and pituitary-thyroid axis hormones characterized by reduced basal testosterone and PRL levels and increased TSH levels. However, since concentrations of these hormones measured at the end of the 240-min hypoglycemic clamp were not affected by TSD it can be speculated that the influence of TSD on the two endocrine axes is rather short lived or does not interact in an additive manner with their responses to hypoglycemia.
PLoS ONE 01/2013; 8(1):e54209. · 4.09 Impact Factor
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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.
Pharmaceutical Research 11/2012; · 4.09 Impact Factor
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ABSTRACT: AIMS: Recurrent hypoglycaemia leads to an attenuation of hypoglycaemic symptoms and hormonal counterregulatory responses. This phenomenon poses a severe problem in the treatment of patients with diabetes mellitus, but the underlying neuroendocrine mechanisms are unclear. Based on animal experimental findings, we hypothesized that counterregulatory attenuation represents a basic adaptive learning process relying on synaptic long-term potentiation or depression. If so, attenuation should be prevented by blocking glutamatergic N-methyl-D-aspartate (NMDA) receptors. MATERIALS AND METHODS: Sixteen healthy young men participated in two conditions, separated by 4 weeks. Participants received the NMDA antagonist memantine over 5 days (15mg/d) in one condition and placebo in the other one. After 3 days of drug administration, participants underwent two hypoglycaemic clamps on day 4 and another one on day 5. We assessed blood concentrations of counterregulatory hormones (cortisol, ACTH, epinephrine, norepinephrine, GH, glucagon) as well as subjective symptoms of hypoglycaemia and word-list recall as an indicator of short-term memory. RESULTS: Counterregulatory responses of all hormones as well as neuroglycopenic and autonomic symptom ratings showed robust attenuation following the third as compared to the first hypoglycaemia (P<0.05). NMDA receptor antagonisation by memantine impaired memory function but did not alter any neuroendocrine measure of counterregulatory attenuation (P>0.17). CONCLUSIONS: Attenuation of the endocrine as well as symptomatic counterregulatory response to recurrent hypoglycaemia is not prevented by the NMDA receptor blocker memantine. Our results do not support the view that adaptation to repeated hypoglycaemia relies on NMDA receptor-mediated plastic processes involving long-term potentiation or depression.
Diabetes Obesity and Metabolism 10/2012; · 3.38 Impact Factor
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ABSTRACT: Cerebral insulin exerts anorexic effects in humans and animals. The underlying mechanisms, however, are not clear. Because insulin physiologically facilitates glucose uptake by most tissues of the body and thereby fosters intracellular energy supply, we hypothesized that intranasal insulin reduces food consumption via enhancement of the neuroenergetic level. In a double-blind, placebo-controlled, within-subject comparison, 15 healthy men (BMI 22.2 ± 0.37 kg/m(2)) aged 22-28 years were intranasally administered insulin (40 IU) or placebo after an overnight fast. Cerebral energy metabolism was assessed by (31)P magnetic resonance spectroscopy. At 100 min after spray administration, participants consumed ad libitum from a test buffet. Our data show that intranasal insulin increases brain energy (i.e., adenosine triphosphate and phosphocreatine levels). Cerebral energy content correlates inversely with subsequent calorie intake in the control condition. Moreover, the neuroenergetic rise upon insulin administration correlates with the consecutive reduction in free-choice calorie consumption. Brain energy levels may therefore constitute a predictive value for food intake. Given that the brain synchronizes food intake behavior in dependence of its current energetic status, a future challenge in obesity treatment may be to therapeutically influence cerebral energy homeostasis. Intranasal insulin, after optimizing its application schema, seems a promising option in this regard.
Diabetes 05/2012; 61(9):2261-8. · 8.29 Impact Factor
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ABSTRACT: Sleep loss has been shown to reduce secretory activity of the pituitary-gonadal axis in men, but the determinants of this effect are unknown.
To discriminate the effects of sleep duration and sleep timing on serum concentrations of luteinizing hormone (LH), testosterone (T) and prolactin (PRL).
Fifteen young, healthy men (27·1 ± 1·3 years; BMI, 22·9 ± 0·3 kg/m(2) ) were examined in a condition of sleep time restriction to 4 h (bedtime, 02:45 -07:00 h) for two consecutive nights and in a control condition of 8 h regular sleep (bedtime, 22:45-07:00 h). After the second night, serum concentrations of LH, T and PRL were monitored over a 15-h period. In addition, these hormones were measured in serum samples obtained in a further experiment in eight healthy men (24·5 ± 1·1 years; BMI, 23·7 ± 0·6 kg/m(2) ) in the morning after one night of total sleep deprivation, of 4·5 h sleep (bedtime, 22:30-03:30 h), and of regular 7 h sleep (bedtime, 22:30-06:00 h).
Serum LH, T and PRL concentrations showed characteristic diurnal variations across the 15-h period without any differences between the 4- and 8-h sleep conditions. However, total sleep deprivation and 4·5 h of sleep restricted to the first night-half markedly decreased morning T and PRL concentrations (both P ≤ 0·05).
Collectively, our data suggest that the effect of sleep restriction on pituitary-gonadal secretory activity may be modulated by sleep timing. While sleep loss in the early part of the night does not affect T and PRL, early awakening and wakefulness during the second part of the night reduces morning circulating T and PRL concentrations.
Clinical Endocrinology 05/2012; 77(5):749-54. · 3.17 Impact Factor
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Tina Sartorius,
Caroline Ketterer,
Stephanie Kullmann,
Michelle Balzer,
Carola Rotermund,
Sonja Binder, Manfred Hallschmid,
Jürgen Machann,
Fritz Schick,
Veronika Somoza,
Hubert Preissl,
Andreas Fritsche,
Hans-Ulrich Häring,
Anita M Hennige
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ABSTRACT: Fat and physical inactivity are the most evident factors in the pathogenesis of obesity, and fat quality seems to play a crucial role for measures of glucose homeostasis. However, the impact of dietary fat quality on brain function, behavior, and sleep is basically unknown. In this study, mice were fed a diet supplemented with either monounsaturated fatty acids (MUFAs) or saturated fatty acids (SFAs) and their impact on glucose homeostasis, locomotion, brain activity, and sleep behavior was evaluated. MUFAs and SFAs led to a significant increase in fat mass but only feeding of SFAs was accompanied by glucose intolerance in mice. Radiotelemetry revealed a significant decrease in cortical activity in SFA-mice whereas MUFAs even improved activity. SFAs decreased wakefulness and increased non-rapid eye movement sleep. An intracerebroventricular application of insulin promoted locomotor activity in MUFA-fed mice, whereas SFA-mice were resistant. In humans, SFA-enriched diet led to a decrease in hippocampal and cortical activity determined by functional magnetic resonance imaging techniques. Together, dietary intake of MUFAs promoted insulin action in the brain with its beneficial effects for cortical activity, locomotion, and sleep, whereas a comparable intake of SFAs acted as a negative modulator of brain activity in mice and humans.
Diabetes 04/2012; 61(7):1669-79. · 8.29 Impact Factor
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Christian Benedict,
Samantha J Brooks,
Owen G O'Daly,
Markus S Almèn,
Arvid Morell,
Karin Åberg,
Malin Gingnell,
Bernd Schultes, Manfred Hallschmid,
Jan-Erik Broman,
Elna-Marie Larsson,
Helgi B Schiöth
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ABSTRACT: 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.
Our objective was to examine brain activation after sleep and sleep deprivation in response to images of food.
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.
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.
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.
The Journal of clinical endocrinology and metabolism 03/2012; 97(3):E443-7. · 6.50 Impact Factor
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ABSTRACT: The role of brain insulin signaling in the control of food intake in humans has not been thoroughly defined. We hypothesized that the hormone contributes to the postprandial regulation of appetite for palatable food, and assessed the effects on appetite and snack intake of postprandial versus fasted intranasal insulin administration to the brain in healthy women. Two groups of subjects were intranasally administered 160 IU insulin or vehicle after lunch. Two hours later, consumption of cookies of varying palatability was measured under the pretext of a taste test. In a control study, the effects of intranasal insulin administered to fasted female subjects were assessed. Compared with placebo, insulin administration in the postprandial but not in the fasted state decreased appetite as well as intake and rated palatability of chocolate chip cookies (the most palatable snack offered). In both experiments, intranasal insulin induced a slight decrease in plasma glucose but did not affect serum insulin concentrations. Data indicate that brain insulin acts as a relevant satiety signal during the postprandial period, in particular reducing the intake of highly palatable food, and impacts peripheral glucose homeostasis. Postprandial intranasal insulin administration might be useful in curtailing overconsumption of snacks with accentuated rewarding value.
Diabetes 02/2012; 61(4):782-9. · 8.29 Impact Factor
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ABSTRACT: Considering that lactate is known to interact with central glucose-sensing networks, we tested whether hyperlactatemia affects food intake in humans. According to a balanced within-subject 2×2 design, 12 healthy, fasted men (age: 20-40 years; BMI: 20-26 kg/m(2)) were intravenously infused lactate and saline, respectively, for 105 min during concomitant euglycemic and hypoglycemic, respectively, insulin infusion of 75 min. Ten minutes after the simultaneous end of infusions, free-choice food intake was assessed at 10:25 h. Lactate decreased food intake following euglycemia as compared to the other three conditions in which food intake did not differ. Results point to an anorexigenic effect of lactate under euglycemic conditions.
Appetite 01/2012; 58(3):818-21. · 2.59 Impact Factor
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ABSTRACT: During psychosocial stress, the brain demands extra energy from the body to satisfy its increased needs. For that purpose it uses a mechanism referred to as "cerebral insulin suppression" (CIS). Specifically, activation of the stress system suppresses insulin secretion from pancreatic beta-cells, and in this way energy-particularly glucose-is allocated to the brain rather than the periphery. It is unknown, however, how the brain of obese humans organizes its supply and demand during psychosocial stress. To answer this question, we examined 20 obese and 20 normal weight men in two sessions (Trier Social Stress Test and non-stress control condition followed by either a rich buffet or a meager salad). Blood samples were continuously taken and subjects rated their vigilance and mood by standard questionnaires. First, we found a low reactive stress system in obesity. While obese subjects showed a marked hormonal response to the psychosocial challenge, the cortisol response to the subsequent meal was absent. Whereas the brains of normal weight subjects demanded for extra energy from the body by using CIS, CIS was not detectable in obese subjects. Our findings suggest that the absence of CIS in obese subjects is due to the absence of their meal-related cortisol peak. Second, normal weight men were high reactive during psychosocial stress in changing their vigilance, thereby increasing their cerebral energy need, whereas obese men were low reactive in this respect. Third, normal weight subjects preferred carbohydrates after stress to supply their brain, while obese men preferred fat and protein instead. We conclude that the brain of obese people organizes its need, supply, and demand in a low reactive manner.
Frontiers in Neuroenergetics 01/2012; 4:4.
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ABSTRACT: 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.
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. Intervention: Fourteen 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.
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).
Serum 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.
The Journal of clinical endocrinology and metabolism 11/2011; 97(2):E218-22. · 6.50 Impact Factor
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ABSTRACT: Circulating concentrations of the orexigenic hormone ghrelin show a postprandial decrease in dependence on meal size and composition. Cognitive determinants of postprandial ghrelin suppression in humans are largely unexplored. We assessed the effects of cued meal anticipation on pre- and postprandial concentrations of total plasma ghrelin, pancreatic polypeptide and leptin as well as on markers of glucose metabolism in healthy men. In a between-subject comparison, meal anticipation was induced in 14 fasted men at 08:00 h by the announcement and subsequent presentation of a breakfast buffet. Fifteen fasted control subjects were informed that they would remain fasted until noon. At 10:00 h, both groups were served a rich free-choice breakfast. At 12:00 h, all subjects underwent a snack test assessing casual cookie intake. Circulating concentrations of ghrelin, pancreatic polypeptide, glucose, insulin and leptin were frequently assessed. Preprandial endocrine parameters as well as breakfast intake (all p>0.23) and subsequent snack consumption (p>0.83) were comparable between groups. The postprandial suppression of ghrelin levels observed in both groups was markedly stronger in subjects who had anticipated breakfast intake (p<0.03) while pancreatic polypeptide concentrations did not differ between groups (p>0.56). Results indicate that meal anticipation is a critical determinant of postprandial ghrelin suppression that, as suggested by unaltered pancreatic polypeptide levels, appears to be mediated independent of vagal activation. Our findings highlight the role of subtle cognitive factors in the postprandial regulation of ghrelin secretion, suggesting that neurobehavioral approaches to improved food intake control should take into account meal anticipatory mechanisms.
Psychoneuroendocrinology 11/2011; 37(7):1096-100. · 5.81 Impact Factor
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ABSTRACT: Reports of increased circulating fibroblast growth factor 21 (FGF21) levels in obesity indicate that FGF21 may be implicated in body weight homeostasis. We sought to investigate the existence of FGF21 in human cerebrospinal fluid (CSF) and, if present, the relationship between CSF FGF21 with body adiposity and metabolic parameters.
CSF and corresponding plasma FGF21 were measured by an enzyme-linked immunosorbent assay (18 men and 20 women, aged 19-80 years, and BMI 16.2-38.1 kg/m(2)) and correlated to body adiposity and metabolic parameters.
CSF and plasma FGF21 increased in particular with rising BMI and fat mass. In CSF, FGF21 was detectable at concentrations ~40% that of plasma levels. CSF and plasma FGF21 levels were significantly positively correlated with BMI and fat mass, body weight, plasma insulin, and homeostasis model assessment of insulin resistance. Plasma FGF21 levels were significantly negatively correlated with plasma adiponectin. When subjected to multiple regression analysis, only fat mass was predictive of plasma FGF21 (β = 0.758; P = 0.004) and CSF FGF21 (β = 0.767; P = 0.007). The CSF-to-plasma FGF21 ratio was significantly negatively correlated with BMI, fat mass, and plasma FGF21. Subjects in the highest plasma FGF21 quintile had a lower CSF-to-plasma FGF21 ratio (12.7% [9.7-14.9%]) compared with those in the lowest plasma FGF21 quintile (94.7% [37.3-99.8%]) (P < 0.01).
Our observations have important implications with respect to the potential central actions of FGF21. Future research should seek to clarify whether FGF21 would be beneficial in the management of obesity and its metabolic complications.
Diabetes 09/2011; 60(11):2758-62. · 8.29 Impact Factor
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ABSTRACT: In recent years, the central nervous system (CNS) has emerged as a principal site of insulin action. This notion is supported by studies in animals relying on intracerebroventricular insulin infusion and by experiments in humans that make use of the intranasal pathway of insulin administration to the brain. Employing neurobehavioural and metabolic measurements as well as functional imaging techniques, these studies have provided insight into a broad range of central and peripheral effects of brain insulin. The present review focuses on CNS effects of insulin administered via the intranasal route on cognition, in particular memory function, and whole-body energy homeostasis including glucose metabolism. Furthermore, evidence is reviewed that suggests a pathophysiological role of impaired brain insulin signaling in obesity and type 2 diabetes, which are hallmarked by peripheral and possibly central nervous insulin resistance, as well as in conditions such as Alzheimer's disease where CNS insulin resistance might contribute to cognitive dysfunction.
Diabetes Obesity and Metabolism 08/2011; 14(3):214-21. · 3.38 Impact Factor
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ABSTRACT: The anticipation of food intake comprises endocrine changes that according to animal experiments include a rise in HPA axis activity. In humans, HPA axis responses to food anticipation and withdrawal, although of clinical relevance, have not been thoroughly examined. We assessed neuroendocrine and psychological effects of food anticipation and of withholding anticipated food in healthy human subjects. Food anticipation was induced in 14 men at 0800 h by the announcement and subsequent presentation of a breakfast buffet. The expected meal was surprisingly withheld at 1000 h under the pretense of an organizational problem. Fifteen fasted controls were informed at 0800 h that they would remain fasted throughout the experiments. In both groups, hunger, mood and circulating concentrations of glucose, insulin, cortisol, ACTH, leptin and ghrelin were assessed. At 1200 h, all subjects were allowed to eat from a plate of cookies. Compared to non-anticipation, food anticipation was associated with a relative increase in serum cortisol levels, an acute drop in plasma glucose and increased self-rated hunger. When anticipated food was withheld, self-rated mood deteriorated and cortisol levels remained elevated, while plasma glucose levels decreased with a delay of 50 min. Other endocrine parameters and cookie intake were comparable between groups. Our results indicate that food anticipation without subsequent food reward increases cortisol levels and reduces blood glucose availability. They support the assumption that dietary restraint, being associated with habitually extended periods of anticipating food that is temporarily withheld, may contribute to the development of overweight by detrimental effects on HPA-axis activity.
Physiology & Behavior 07/2011; 103(5):594-9. · 2.87 Impact Factor
