peptide-yy and Weight-Gain

The gastrointestinal (GI) tract is a specialized sensory system that detects and responds to constant changes in nutrient- and bacterial-derived intestinal signals, thus contributing to controls of food intake. Chronic exposure to dietary fat causes morphological, physiological and metabolic changes leading to disruptions in the regulatory feeding pathways promoting more efficient fat absorption and utilization, blunted satiation signals and excess adiposity. Accumulating evidence demonstrates that impaired gastrointestinal signals following long-term high fat consumption are, at least partially, responsible for increased caloric intake. This review focuses on the role of dietary fat in modulating oral and post-oral chemosensory signaling elements responsible for lipid detection and responses, including changes in sensitivity to satiation signals, such as GLP-1, PYY and CCK and their impact on food intake and weight gain. Furthermore, the influence of the gut microbiota on mechanisms controlling energy regulation in the face of excessive fat exposure will be explored. The profound influence of dietary fats on altering complex regulatory feeding pathways can result in dysregulation of body weight and development of obesity, while restoration or manipulation of satiation signaling may prove an effective tool in prevention and treatment of obesity.

Topics: Adiposity; Animals; CD36 Antigens; Cholecystokinin; Dietary Fats; Energy Intake; Gastrointestinal Tract; Ghrelin; Glucagon-Like Peptide 1; Humans; Intestinal Absorption; Microbiota; Obesity; Peptide YY; Receptors, G-Protein-Coupled; Satiation; Signal Transduction; Taste; Weight Gain

Ghrelin is a peptide hormone secreted into circulation from the stomach. It has been postulated to act as a signal of hunger. Ghrelin administration acutely increases energy intake in lean and obese humans and chronically induces weight gain and adiposity in rodents. Circulating ghrelin levels are elevated by fasting and suppressed following a meal. Inhibiting ghrelin signaling therefore appears an attractive target for anti-obesity therapies. A number of different approaches to inhibiting the ghrelin system to treat obesity have been explored. Despite this, over a decade after its discovery, no ghrelin based anti-obesity therapies are close to reaching the market. This article discusses the role of ghrelin in appetite control in humans, examines different approaches to inhibiting the ghrelin system and assesses their potential as anti-obesity therapies.

Topics: Acyltransferases; Adipose Tissue; Adiposity; Animals; Antibodies, Neutralizing; Appetite; Appetite Regulation; Eating; Fasting; Ghrelin; Humans; Hunger; Mice; Obesity; Peptide Hormones; Peptide YY; Peptides; Rats; Receptors, Ghrelin; Satiety Response; Substance P; Weight Gain

Amylin is a pancreatic B-cell hormone that plays an important role in the control of nutrient fluxes because it reduces food intake, slows gastric emptying, and reduces postprandial glucagon secretion. These actions seem to depend on a direct effect on the area postrema (AP). Subsequent to area AP activation, the amylin signal is conveyed to the forebrain via distinct relay stations. Within the lateral hypothalamic area, amylin diminishes the expression of orexigenic neuropeptides. Recent studies suggest that amylin may also play a role as a long term, adiposity signal. Similar to leptin or insulin, an infusion of amylin into the brain resulted in lower body weight gain than in controls, irrespective of the starting body weight. Interestingly, preliminary data also suggest that rats fed an energy-dense diet develop resistance to central amylin. In addition to amylin's action to control meal termination and to act as a potential adiposity signal, amylin and its agonist salmon calcitonin have recently been shown to increase energy expenditure under certain conditions. In summary, amylin may be an interesting target as a body weight lowering drug. In fact, recent studies provide evidence that amylin, especially when combined with other anorectic hormones (for example, peptide YY and leptin) has beneficial long-term effects on body weight.

Topics: Adiposity; Amyloid; Animals; Appetite Depressants; Appetite Regulation; Area Postrema; Dose-Response Relationship, Drug; Energy Metabolism; Feeding Behavior; Humans; Islet Amyloid Polypeptide; Leptin; Obesity; Peptide YY; Proto-Oncogene Proteins c-fos; Rats; Satiety Response; Weight Gain

Roux-en-Y gastric bypass (RYGB) produces rapid and dramatic weight loss in very heavy obese patients. Up to 20% cannot sustain their weight loss beyond 2 to 3 y after surgery.. To identify putative etiologic factors producing post-RYGB weight regain, a literature survey of metabolic changes in very obese and a review of our diet-induced obese RYGB rat model data was done.. Weight regain suggests an imbalance in physiologic mechanisms regulating appetite and metabolic rate. Weight regain occurred in 25% of our rats, produced by return to presurgical energy intake levels. The 75% of rats that sustained weight loss secreted a significantly larger amount of peptide YY (PYY) while suppressing leptin secretion; those that failed were unable to develop or sustain a sufficiently large plasma PYY:leptin ratio. Metabolic consequences of this failure included reversal of initial postsurgical increases in peripheral fatty acid oxidation, anorexigenic activity in the hypothalamic arcuate nucleus and paraventricular nucleus, and the expression of uncoupling protein-2 in adipose tissues, and decreases in hepatic lipogenesis, free tri-iodothyronine secretion, expression of orexigenic activity in the arcuate nucleus and paraventricular nucleus, expression of adenosine monophosphate kinase in adipose tissues, skeletal muscle mitochondrial mass, and endocannabinoid content and appetite.. Weight regain after RYGB occurs in approximately 20% of patients and constitutes a serious complication. Weight regain-promoting consequences are attributed to a failure to sustain elevated plasma PYY concentrations, indicating that combining RYGB with pharmacologic stimulation of PYY secretion in patients after RYGB who exhibit inadequate PYY concentration may increase long-term success of surgical weight reduction in morbidly obese adults.

Topics: Adipose Tissue; Animals; Energy Metabolism; Fatty Acids; Feeding Behavior; Gastric Bypass; Humans; Hypothalamus; Leptin; Peptide YY; Rats; Recurrence; Weight Gain

Anorexia nervosa (AN) initiates an adaptive response at the level of the hypothalamus, which results in a complex interplay involving most elements of the neuroendocrine axis. Consequences of onset of disease in adolescence include amenorrhoea, pubertal arrest with potential loss of target height, and osteoporosis with reduced capacity for future attainment of peak bone mass. With recovery, delay in restoration of menses is common. Hormonal therapies for restoration of bone mineral density (BMD) in adolescents have shown limited efficacy. This review will discuss the reproductive endocrine effects of AN in adolescence, and discuss new investigative tools for monitoring restoration of reproductive function and BMD in this population.

Topics: Adolescent; Anorexia Nervosa; Bone Density; Bone Density Conservation Agents; Bone Diseases; Bone Resorption; Calcium; Dehydroepiandrosterone; Diphosphonates; Estrogen Replacement Therapy; Exercise Therapy; Female; Ghrelin; Humans; Hypothalamo-Hypophyseal System; Insulin-Like Growth Factor I; Leptin; Ovary; Peptide YY; Pituitary-Adrenal System; Reproductive Medicine; Vitamin D; Weight Gain

Peptide YY (PYY) is a 36 amino acid, straight chain polypeptide, which is co-localized with GLP-1 in the L-type endocrine cells of the GI mucosa. PYY shares structural homology with neuropeptide Y (NPY) and pancreatic polypeptide (PP), and together form the Neuropeptide Y Family of Peptides, which is also called the Pancreatic Polypeptide-Fold Family of Peptides. PYY release is stimulated by intraluminal nutrients, including glucose, bile salts, lipids, short-chain fatty acids and amino acids. Regulatory peptides such as cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), gastrin and GLP-1 modulate PYY release. The proximal GI tract may also participate in the regulation of PYY release through vagal fibers. After release, dipeptidyl peptidase IV (DPP-IV; CD 26) cleaves the N-terminal tyrosine-proline residues forming PYY(3-36). PYY(1-36) represents about 60% and PYY(3-36) 40% of circulating PYY. PYY acts through Y-receptor subtypes: Y1, Y2, Y4 and Y5 in humans. PYY(1-36) shows high affinity to all four receptors while PYY(3-36) is a specific Y2 agonist. PYY inhibits many GI functions, including gastric acid secretion, gastric emptying, small bowel and colonic chloride secretion, mouth to cecum transit time, pancreatic exocrine secretion and pancreatic insulin secretion. PYY also promotes postprandial naturesis and elevates systolic and diastolic blood pressure. PYY(1-36) and PYY(3-36) cross the blood-brain barrier and participate in appetite and weight control regulation. PYY(1-36) acting through Y1- and Y5-receptors increases appetite and stimulates weight gain. PYY(3-36) acting through Y2-receptors on NPY-containing cells in the arcuate nucleus inhibits NPY release and, thereby, decreases appetite and promotes weight loss. PYY may play a primary role in the appetite suppression and weight loss observed after bariatric operations.

Topics: Adenosine Deaminase; Animals; Appetite; Arcuate Nucleus of Hypothalamus; Dipeptidyl Peptidase 4; Gastrointestinal Tract; Glucagon-Like Peptides; Glycoproteins; Humans; Kidney; Peptide Fragments; Peptide YY; Weight Gain

Rosiglitazone often results in weight gain. We hypothesized that rosiglitazone may modulate circulating levels of ghrelin and peptide YY(3-36) and this modulation may be related to weight-gaining effect of this agent. This study was designed as an open-label, randomized, controlled trial of 3-month duration. Women with newly diagnosed type 2 diabetes were studied. Twenty-eight of the 55 eligible participants were randomly assigned to receive rosiglitazone (4 mg/d). Twenty-seven patients with diabetes matched for age and body mass index served as controls on diet alone. We evaluated the effects of 3 months of rosiglitazone treatment on fasting peptide YY(3-36) and ghrelin levels, and anthropometric measurements. The 3-month administration of rosiglitazone reduced fasting plasma peptide YY(3-36) levels by 25%, the between-group difference was statistically significant. No effect of this thiazolidinedione compound on fasting ghrelin concentrations was observed at the end of study. The ghrelin/body mass index ratio also did not change significantly after treatment. Seventy-five percent of the women with diabetes complained of increased hunger at the end of study. Nevertheless, all subjects exhibited a decrease in fasting PYY levels after 3 months of rosiglitazone therapy, irrespective of the levels of hunger. There was no significant correlation between changes in peptide YY(3-36) and those in anthropometric parameters and insulin sensitivity at the end of the study. Rosiglitazone-induced decrease in fasting peptide YY(3-36) levels may in part contribute to orexigenic and weight-gaining effect of this thiazolidinedione derivative.

Topics: Adult; Aged; Diabetes Mellitus, Type 2; Down-Regulation; Fasting; Female; Humans; Middle Aged; Peptide YY; Rosiglitazone; Thiazolidinediones; Weight Gain

The SHAPE (Screened Health Assessment and Pacer Evaluation) trial was a 24 month randomized multicenter placebo-controlled study to determine the efficacy of an implantable gastric stimulator (IGS) for weight loss. This report is an investigator-initiated sub-study at one site designed to assess whether IGS affects plasma levels of ghrelin and peptide YY (PYY). The device was implanted in all subjects but was activated in the TREATMENT group (n = 7, BMI = 41.5 ± 2.0 kg/m2) and remained inactive in the CONTROL (n = 6, BMI = 39.5 ± 1.7 kg/m2) during the first 12 months. IGS was activated in both groups during months 12-24. Fasting venous blood was drawn at months 0, 12, and 24 and an oral glucose tolerance test (OGTT) was performed at month 12. Although there was no difference in weight loss at 6 months (. -6.6 ± 1.5% vs.. -6.2 ± 1.4%), at 24 months the CONTROL group exhibited weight gain from baseline (+2.2 ± 1.5%) that was significantly different from the weight loss in the TREATMENT group (-1.9 ± 1.4%; P < 0.05). At 12 months, fasting ghrelin was significantly increased (P < 0.05) in the TREATMENT group (285 ± 35 to 336 ± 35 pg/ml; weight change, -4.9 ± 1.4%), but not in the CONTROL (211 ± 36 to 208 ± 35 pg/ml; weight change, -3.4 ± 1.5%). No significant change was observed in postprandial suppression of plasma ghrelin or in fasting and postprandial PYY levels. In conclusion, IGS does not prevent the increase in fasting plasma ghrelin levels associated with weight loss. Further studies are needed to determine whether changes in technology can improve weight loss and maintenance, perhaps using gut hormones as biomarkers of possible efficacy.

Topics: Adolescent; Adult; Aged; Double-Blind Method; Electric Stimulation; Electrodes, Implanted; Fasting; Female; Ghrelin; Glucose Tolerance Test; Humans; Male; Middle Aged; Obesity, Morbid; Peptide YY; Postprandial Period; Weight Gain; Weight Loss; Young Adult

Epidemiological evidence shows an inverse relationship between dietary fibre intake and body weight gain. Oat beta-glucan, a soluble fibre alters appetite hormones and subjective satiety in acute meal test studies, but its effects have not been demonstrated with chronic consumption. The present study aimed to test the effects in women of two different doses of oat beta-glucan on weight loss and hormones associated with appetite regulation. In a 3-month parallel trial, sixty-six overweight females were randomised into one of three 2 MJ energy-deficit diets: a control and two interventions including 5-6 g or 8-9 g beta-glucan. Anthropometric and metabolic variables (blood glucose level, insulin, total cholesterol (TC), LDL, HDL, TAG and leptin), together with markers of appetite regulation (cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), ghrelin, peptide YY (PYY) and PYY3-36) were measured at baseline and at 3 months. After 3 months, all groups lost weight (P < 0.001) and showed a reduced waist circumference (P < 0.001). The study sample also showed reductions in TC, LDL, HDL, leptin, PYY, GLP-1 values (all P < 0.001) and an increase in CCK levels (P < 0.001). No significant differences were noted between the groups for all outcome values except PYY levels (P = 0.018). In broad terms, the addition of oat beta-glucan did not enhance the effect of energy restriction on weight loss in mildly overweight women, although wide variations in observed results suggests that individual responsiveness may be an issue.

Topics: Adult; Appetite; Avena; beta-Glucans; Blood Glucose; Body Mass Index; Cholesterol; Diet, Reducing; Dietary Fiber; Dietary Supplements; Dose-Response Relationship, Drug; Female; Ghrelin; Hormones; Humans; Insulin; Lipoproteins; Overweight; Peptide YY; Satiation; Weight Gain

The role of fat-free mass loss (FFML) in modulating weight regain in individuals with obesity, as well as the potential mechanisms involved, remain inconsistent.. The aim of this study was to determine if % FFML following weight loss (WL) is a predictor of weight regain and to investigate the association between %FFML and changes in appetite markers.. WL at week 9 was 17.5 ± 4.3kg and %FFML 20.4 ± 10.6%. Weight regain at 1 y was 1.7 ± 8.2 kg (8.8 ± 45.0%). After adjusting for WL and fat mass at baseline, %FFML at week 9 was not a significant predictor of weight regain. Similar results were seen at week 13. The greater the %FFML at week 9, but not 13, the smaller the reduction, or greater the increase in basal ghrelin concentration (β: -3.2; 95% CI: -5.0, -1.1; P = 0.003), even after adjusting for WL and β-hydroxybutyrate.. %FFML was not a significant predictor of weight regain at 1 y in individuals with obesity. However, a greater %FFML was accompanied by a greater increase in ghrelin secretion under ketogenic conditions, suggesting a link between fat-free mass and appetite regulation. This trial was registered at clinicaltrials.gov as NCT01834859.

Topics: 3-Hydroxybutyric Acid; Adult; Appetite; Ghrelin; Humans; Male; Middle Aged; Obesity; Peptide YY; Weight Gain; Weight Loss

TOTUM-63, a fibre and polyphenol rich plant-based composition, has been demonstrated to significantly improve body weight and glucose homeostasis in animal models of obesity. Our study aimed at exploring whether the mechanisms include modulation of gut (glucose-dependent insulinotropic peptide (GIP), glucagon-like petide-1 (GLP-1), cholecystokinin (CCK), peptide YY (PYY)) and pancreatic (insulin, glucagon) hormones, all important regulators of glucose control, appetite and body weight.. Male C57BL/6JRJ mice were assigned to either standard chow (CON), high fat diet (HF, 60% energy from fat) or HF-TOTUM-63 (HF diet 60% supplemented with TOTUM-63 2.7%) for 10 weeks. In vivo glucose homeostasis (oral glucose tolerance test (OGTT), intraperitoneal pyruvate tolerance test (ipPTT)), glucose-induced portal vein hormone concentration, gut hormone gene expression and protein content as well as enteroendocrine cell contents were assessed at the end of the dietary intervention. The present study evidenced that TOTUM-63 reduced food intake, limited weight gain and improved glucose and pyruvate tolerance of HF-fed animals. This was associated with an increase in PYY content in the colon, an altered pattern of PYY secretion between fasted and glucose-stimulated states, and with a significant improvement in the portal vein concentration of GLP-1, insulin and glucagon, but not GIP and CCK, in response to glucose stimulation.. Overall, these data suggest that TOTUM-63 might have a specific impact on gut L-cells and on the expression and secretion of GLP-1 and PYY incretins, potentially contributing to the reduced food intake, body weight gain and improved glucose homeostasis.

Topics: Animals; Blood Glucose; Body Weight; Diet, High-Fat; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Humans; Insulin; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Peptide YY; Plant Extracts; Polyphenols; Pyruvates; Weight Gain

Obesity is a common disease worldwide and there is an urgent need for strategies to preventing obesity.. The anti-obesity effect and mechanism of Ligilactobacillus salivarius LCK11 (LCK11) is studied using a C57BL/6J male mouse model in which obesity is induced by a high-fat diet (HFD). Results show that LCK11 can prevent HFD-induced obesity, reflected as inhibited body weight gain, abdominal and liver fat accumulation and dyslipidemia. Analysis of its mechanism shows that on the one hand, LCK11 can inhibit food intake through significantly improving the transcriptional and translational levels of peptide YY (PYY) in the rectum, in addition to the eventual serum PYY level; this is attributed to the activation of the toll-like receptor 2/nuclear factor-κB signaling pathway in enteroendocrine L cells by the peptidoglycan of LCK11. On the other hand, LCK11 supplementation effectively reduces the Firmicutes/Bacteroidetes ratio and shifts the overall structure of the HFD-disrupted gut microbiota toward that of mice fed on a low-fat diet; this also contributes to preventing obesity.. LCK11 shows the potential to be used as a novel probiotic for preventing obesity by both promoting PYY secretion to inhibit food intake and regulating gut microbiota.

Topics: Adipose Tissue; Animals; Anti-Obesity Agents; Diet, High-Fat; Dyslipidemias; Eating; Enteroendocrine Cells; Gastrointestinal Microbiome; Intestines; Lactobacillaceae; Liver; Male; Mice, Inbred C57BL; Obesity; Peptide YY; Probiotics; Weight Gain

Roux-en-Y gastric bypass (RYGB) is one of the most effective surgical therapies for the rapid resolution of type 2 diabetes. However, the mechanisms underlying the entero-hormonal response after surgery and the role of peptide tyrosine tyrosine (PYY) in the restoration of normoglycemia are still not clear.. We reproduced the RYGB technique in Wistar and Goto-Kakizaki rats and performed serum hormonal, histological, and hormonal-infusion test.. Using the diabetic Goto-Kakizaki (GK) rat model, we demonstrated that PYY plasma levels showed a remarkable peak approximately 30 min earlier than GLP-1 or GIP after mixed-meal administration in RYGB-operated rats with PYY. The GLP-1 and GIP areas under the curve (AUCs) increased after RYGB in GK rats. Additionally, the findings suggested that PYY (3-36) infusion led to increased GLP-1 and GIP plasma levels close to those obtained after a meal. Finally, the number of GLP-1-positive cells appeared to increase in the three segments of the small intestine in GK-RYGB-operated rats beyond the early presence of nutrient stimulation in the ileum. Nevertheless, PYY-positive cell numbers appeared to increase only in the ileum.. At least in rats, these data demonstrate an earlier essential role for PYY in gut hormone regulation after RYGB. We understand that PYY contributes to GLP-1 and GIP release and there must be the existence of enteroendocrine communication routes between the distal and proximal small intestine.

Topics: Animals; Blood Glucose; Diabetes Mellitus, Experimental; Gastric Bypass; Gastrointestinal Hormones; Glucose Tolerance Test; Glycemic Control; Insulin Secretion; Intestinal Mucosa; Intestines; Male; Peptide YY; Rats; Rats, Wistar; Weight Gain

To assess the relationship of body composition measures and basal metabolic rate (BMR) with gastrointestinal hormones in weight regain 5 years after gastric bypass.. A total of 42 patients were divided into two groups: with and without weight regain 5 years after gastric bypass. Hormone assessments were performed after a fasting period and at 30, 60, and 120 min after the standard meal intake.. Patients with no weight regain had significantly lower visceral fat (VF), lower fat body mass (FBM), and lower fat percentage (%F) in relation to the other group. In the group without weight regain, at baseline, glucose-dependent insulinotropic polypeptide (GIP) showed a negative correlation with weight and BMI and a positive correlation with BMR, skeletal muscle mass (SMM), and fat-free mass (FFM). After the standard meal, the following results were found: a negative correlation with %F, a positive correlation of glucagon-like peptide-1 (GLP-1) with FFM, and a positive correlation of GLP-2 and PYY with BMR, SMM, and FFM. In the group with weight regain, at baseline, GIP, PYY, and GLP-1 showed a negative correlation with %F. After the standard meal, PYY and GLP-1 showed a negative correlation with VF, FBM, and %F. On the other hand, GLP-2 negatively correlated with VF and FBM.. It is possible to conclude that there is a different relationship of concentrations of PYY, GIP, GLP-1, and GLP-2 with body composition and BMR in patients with and without weight regain in the late gastric bypass postoperative period.

Topics: Animals; Body Composition; Gastric Bypass; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Humans; Obesity, Morbid; Peptide YY; Weight Gain

Schizophrenia is among the top half of the 25 leading causes of disabilities worldwide with a 10-20 year decrease in life expectancy. Ineffective pharmacotherapy in the management of cognitive deficits and weight gain are known to be significant contributors; therefore interventions that may mitigate one, or both, of these parameters would be highly beneficial. Manipulation of the gut microbiome using dietary supplements such as prebiotics may be one such intervention. Preclinical studies have shown that a 2-4 week dietary supplementation with a prebiotic has beneficial effects on learning and memory, and prevents pro-inflammatory signals that are detrimental to cognitive processes. Furthermore, prebiotics influence metabolism, and in obesity they increase the expression of anorexigenic gut hormones such as peptide tyrosine tyrosine, glucagon-like peptide 1 and leptin, as well as decrease levels of orexigenic hormones such as ghrelin. Despite compelling evidence for the pro-cognitive and neuroprotective effects of prebiotics in rodents, their ability to alleviate cognitive deficits or enhance cognition needs to be evaluated in humans. Here we suggest that important symptoms associated with schizophrenia, such as cognitive impairment and weight gain, may benefit from concurrent prebiotic therapy.

Topics: Cognition; Dietary Supplements; Gastrointestinal Microbiome; Ghrelin; Glucagon-Like Peptide 1; Humans; Leptin; Obesity; Peptide YY; Prebiotics; Schizophrenia; Weight Gain

Diet-induced weight loss (WL) leads to a compensatory increase in appetite and changes in the plasma concentration of appetite-regulating hormones are likely to play a role. Whether these changes are transient or sustained remains unclear. This study aimed to assess if changes in subjective and objective appetite markers observed with WL are sustained after 1 year (1Y).. At Wk13, 16% WL (-18 ± 1 kg, P < 0.001) was associated with a significant increase in fasting and postprandial hunger ratings (P < 0.01 and P < 0.05, respectively), and postprandial fullness (P < 0.01) combined with a reduction in PFC (P < 0.001). These were accompanied by a significant rise in basal and postprandial AG concentrations (P < 0.001, for both), a reduction in postprandial CCK (P < 0.01) and in basal and postprandial insulin (P < 0.001). At 1Y follow-up, with sustained WL (15%; -16 ± 1 kg, P < 0.001), fasting hunger and postprandial fullness ratings remained increased (P < 0.05 for both), and postprandial PFC reduced (P < 0.001). Basal and postprandial AG remained elevated and insulin reduced (P < 0.001, for all), while postprandial CCK was increased (P < 0.01) and PYY decreased (P < 0.001).. With a 15% sustained WL at 1Y, the drive to eat in the fasting state is increased, but this may be balanced out by raised postprandial feelings of fullness. To assist with WL maintenance, new strategies are required to manage increased hunger and drive to eat.

Topics: Adult; Appetite; Body Weight; Diet; Female; Ghrelin; Humans; Longitudinal Studies; Male; Middle Aged; Peptide YY; Postprandial Period; Weight Gain; Weight Loss

Enteroendocrine cells sense nutrients through taste receptors similar to those on the tongue. Sweet and fatty acid taste receptors (FFAR) coupled to the gustatory G-protein, gustducin, on enteroendocrine cells play a role in gut hormone release. We studied if supplementation of artificial (sucralose) or prebiotic (oligofructose; OFS) sweeteners target gustducin-mediated signaling pathways to alter gut hormone release and reduce obesity-associated disorders.. Wild-type (WT) and α-gustducin knockout (α-gust

Topics: Animals; Diet, High-Fat; Dietary Supplements; Enteroendocrine Cells; Gastrointestinal Tract; Ghrelin; Glucagon-Like Peptide 1; Insulin Resistance; Male; Mice, Inbred C57BL; Mice, Knockout; Oligosaccharides; Peptide YY; Receptors, G-Protein-Coupled; Sucrose; Sweetening Agents; Transducin; Weight Gain

Dietary supplementation with fermentable carbohydrate protects against body weight gain. Fermentation by the resident gut microbiota produces short-chain fatty acids, which act at free fatty acid receptor 2 (FFAR2). Our aim was to test the hypothesis that FFAR2 is important in regulating the beneficial effects of fermentable carbohydrate on body weight and to understand the role of gut hormones PYY and GLP-1.. Wild-type or. We provide new mechanistic insight into how fermentable carbohydrate regulates metabolism. Using mice that lack FFAR2, we demonstrate that the fermentable carbohydrate inulin acts via this receptor to drive an 87% increase in the density of cells that produce the appetite-suppressing hormone peptide YY (PYY), reduce food intake, and prevent diet-induced obesity.. Our results demonstrate that FFAR2 is predominantly involved in regulating the effects of fermentable carbohydrate on metabolism and does so, in part, by enhancing PYY cell density and release. This highlights the potential for targeting enteroendocrine cell differentiation to treat obesity.

Topics: Animals; Body Weight; Colon; Dietary Carbohydrates; Dietary Supplements; Eating; Fatty Acids, Volatile; Fermentation; Fermented Foods; Gastrointestinal Hormones; Gastrointestinal Microbiome; Glucagon-Like Peptide 1; Inulin; Male; Mice; Mice, Knockout; Obesity; Peptide YY; Receptors, Cell Surface; Weight Gain

Overnutrition during early development has been linked to metabolic disease and obesity in adulthood. Interventions to ameliorate this metabolic malprogramming are needed. Our objective was to determine whether prebiotic fibre would reduce weight gain and improve satiety hormone profiles in rats overnourished during the suckling period.. Male Sprague-Dawley rats reared in small litter (SL 3 pups) or normal litter (NL 12 pups) were randomized at weaning to AIN-93 (control) or a 10 % oligofructose (OFS) diet for 16 weeks. Body composition, an oral glucose tolerance test for glucose and gut hormones, and gut microbiota were assessed.. At weaning, body weight was higher in SL than in NL rats (P < 0.03). At 19 weeks, body weight was lower with OFS than control (P < 0.04). There was a diet × litter size interaction wherein OFS in SL rats reduced body fat (%) to levels seen in NL rats (P < 0.05). OFS attenuated the glucose response in SL but not in NL rats (P < 0.015). Independent of litter size, OFS decreased total AUC for glucose-dependent insulinotropic polypeptide (P < 0.002) and increased total AUC for peptide YY (P < 0.01) and glucagon-like peptide-1 (P < 0.04) when compared to control. OFS, not litter size, played the predominant role in altering gut microbiota which included increased bifidobacteria and Akkermansia muciniphila with OFS.. Postnatal consumption of OFS by rats raised in SL was able to attenuate body fat and glycaemia to levels seen in NL rats. OFS appears to influence satiety hormone and gut microbiota response similarly in overnourished and control rats.

Topics: Animals; Blood Glucose; Body Composition; Dietary Fiber; Energy Intake; Fatty Acids, Volatile; Gastric Inhibitory Polypeptide; Gastrointestinal Microbiome; Ghrelin; Glucagon-Like Peptide 1; Glucose Tolerance Test; Insulin; Islet Amyloid Polypeptide; Leptin; Male; Oligosaccharides; Organ Size; Overnutrition; Peptide YY; Prebiotics; Rats; Rats, Sprague-Dawley; Weight Gain

In a previous study, we showed that saccharin can induce weight gain when compared with sucrose in Wistar rats despite similar total caloric intake. We now question whether it could be due to the sweet taste of saccharin per se. We also aimed to address if this weight gain is associated with insulin-resistance and to increases in gut peptides such as leptin and PYY in the fasting state. In a 14 week experiment, 16 male Wistar rats received either saccharin-sweetened yogurt or non-sweetened yogurt daily in addition to chow and water ad lib. We measured daily food intake and weight gain weekly. At the end of the experiment, we evaluated fasting leptin, glucose, insulin, PYY and determined insulin resistance through HOMA-IR. Cumulative weight gain and food intake were evaluated through linear mixed models. Results showed that saccharin induced greater weight gain when compared with non-sweetened control (p = 0.027) despite a similar total caloric intake. There were no differences in HOMA-IR, fasting leptin or PYY levels between groups. We conclude that saccharin sweet taste can induce mild weight gain in Wistar rats without increasing total caloric intake. This weight gain was not related with insulin-resistance nor changes in fasting leptin or PYY in Wistar rats.

Topics: Animals; Blood Glucose; Drinking Water; Energy Intake; Fasting; Glucose Transporter Type 2; Insulin; Insulin Resistance; Leptin; Male; Peptide YY; Rats; Saccharin; Taste; Weight Gain; Yogurt

Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.

Topics: Animals; Body Mass Index; Chemokine CCL11; Energy Metabolism; Ghrelin; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Insulin; Intestine, Large; Leptin; Mice, Inbred C57BL; Microbiota; Models, Biological; Peptide Hormones; Peptide YY; Specific Pathogen-Free Organisms; Weight Gain

Hyperemesis gravidarum (HG) is described as unexplained excessive nausea and vomiting during pregnancy. Some gut hormones that regulate appetite may have important role in etiopathogenesis of HG and weight changes during pregnancy. In this study, levels of gut satiety hormones were evaluated in pregnant women with HG.. This prospective case-control study was conducted in 30 women with HG and 30 healthy pregnant women without symptoms of HG. Fasting venous blood samples were taken from all subjects for measurement of plasma gut hormone levels; obestatin (pg/mL), peptide YY (PYY), pancreatic polypeptide (PP) and cholecystokinin (CCK).. Plasma PYY and PP levels were significantly higher in HG group. The most important parameter in diagnosis of HG was plasma PP level. Simple use of PP level led to the diagnosis 91.1 % of HG cases correctly. The single most important parameter in the prediction of HG was also PP level.. Anorexigenic gut hormones might have important role in etiopathogenesis of hyperemesis gravidarum and weight changes during pregnancy.

Topics: Adult; Body Weight; Case-Control Studies; Cholecystokinin; Fasting; Female; Ghrelin; Humans; Hyperemesis Gravidarum; Pancreatic Polypeptide; Peptide YY; Pregnancy; Prospective Studies; Weight Gain; Young Adult

This study aimed to characterise lean and obese phenotypes according to diet and body composition, and to compare fasting and postprandial appetite and metabolic profiles following a high-fat test meal. A total of ten lean (BMI40 and 30 kg/m2) high-fat consumers (OHF; >40 % energy from fat) were recruited. Before and following the test meal (4727 kJ (1130 kcal), 77 % fat, 20 % carbohydrate (CHO) and 3 % protein), fasting plasma glucose, insulin, leptin, ghrelin, peptide YY (PYY), RER, RMR and subjective appetite ratings (AR) were measured for 6 h. Thereafter, subjects consumed a self-selected portion of a standardised post-test meal (40 % fat, 45 % CHO and 15 % protein) and reported AR. Fasting (P=0·01) and postprandial (P<0·001) fat oxidation was significantly higher in LHF than in LLF but was not different between LHF and OHF. Although similar between the lean groups, fasting and postprandial energy expenditures were significantly higher in OHF compared with LHF (P<0·01). Despite similar AR across groups, LLF consumed a relatively greater quantity of the post-test meal than did LHF (7·87 (sd 2·96) v. 7·23 (sd 2·67) g/kg, P=0·013). The lean groups showed appropriate changes in plasma ghrelin and PYY following the test meal, whereas the OHF group showed a blunted response. In conclusion, the LHF phenotype had a greater capacity for fat oxidation, which may be protective against weight gain. OHF individuals had a blunted appetite hormone response to the high-fat test meal, which may subsequently increase energy intake, driving further weight gain.

Topics: Adult; Appetite; Basal Metabolism; Body Composition; Body Mass Index; Diet; Diet, High-Fat; Dietary Fats; Energy Intake; Fasting; Female; Ghrelin; Humans; Obesity; Oxidation-Reduction; Peptide YY; Phenotype; Postprandial Period; Satiation; Surveys and Questionnaires; Thinness; Weight Gain

Eating at a time when the internal circadian clock promotes sleep is a novel risk factor for weight gain and obesity, yet little is known about mechanisms by which circadian misalignment leads to metabolic dysregulation in humans. We studied 14 adults in a 6-d inpatient simulated shiftwork protocol and quantified changes in energy expenditure, macronutrient utilization, appetitive hormones, sleep, and circadian phase during day versus nightshift work. We found that total daily energy expenditure increased by ∼4% on the transition day to the first nightshift, which consisted of an afternoon nap and extended wakefulness, whereas total daily energy expenditure decreased by ∼3% on each of the second and third nightshift days, which consisted of daytime sleep followed by afternoon and nighttime wakefulness. Contrary to expectations, energy expenditure decreased by ∼12-16% during scheduled daytime sleep opportunities despite disturbed sleep. The thermic effect of feeding also decreased in response to a late dinner on the first nightshift. Total daily fat utilization increased on the first and second nightshift days, contrary to expectations, and carbohydrate and protein utilization were reduced on the second nightshift day. Ratings of hunger were decreased during nightshift days despite decreases in 24-h levels of the satiety hormones leptin and peptide-YY. Findings suggest that reduced total daily energy expenditure during nightshift schedules and reduced energy expenditure in response to dinner represent contributing mechanisms by which humans working and eating during the biological night, when the circadian clock is promoting sleep, may increase the risk of weight gain and obesity.

Topics: Adult; Analysis of Variance; Circadian Rhythm; Eating; Electromyography; Energy Metabolism; Female; Ghrelin; Humans; Leptin; Male; Melatonin; Obesity; Peptide YY; Risk Factors; Sleep; Sleep Deprivation; Sleep Stages; Time Factors; Wakefulness; Weight Gain; Work Schedule Tolerance

The presence of appetite hormones, namely glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and leptin in breast milk may be important in infant feeding regulation and infant growth. This study evaluated whether concentrations of GLP-1, PYY, and leptin change across a single feeding (from fore- to hindmilk), and are associated with maternal and infant anthropometrics.. Thirteen postpartum women (mean ± SD: 25.6 ± 4.5 years, 72.0 ± 11.9 kg) provided fore- and hindmilk samples 4-5 weeks after delivery and underwent measurements of body weight and composition by Dual X-ray Absorptiometry. GLP-1, PYY, and leptin concentrations were measured using radioimmunoassay, and milk fat content was determined by creamatocrit.. Concentration of GLP-1 and content of milk fat was higher in hindmilk than foremilk (P ≤ 0.05). PYY and leptin concentrations did not change between fore- and hindmilk. Both leptin concentration and milk fat content were correlated with indices of maternal adiposity, including body mass index (r = 0.65-0.85, P < 0.02), and fat mass (r = 0.65-0.84, P < 0.02). Hindmilk GLP-1 was correlated with infant weight gain from birth to 6 months (r = -0.67, P = 0.034).. The presence of appetite hormones in breast milk may be important in infant appetite and growth regulation.

Topics: Absorptiometry, Photon; Adiposity; Adult; Appetite; Body Mass Index; Female; Glucagon-Like Peptide 1; Humans; Leptin; Milk, Human; Peptide YY; Postpartum Period; Radioimmunoassay; Weight Gain; Young Adult

Obesity and its associated conditions such as type 2 diabetes mellitus are major causes of morbidity and mortality. The iminosugar N-(5-adamantane-1-yl-methoxy-pentyl)-deoxynojirimycin (AMP-DNM) improves insulin sensitivity in rodent models of insulin resistance and type 2 diabetes mellitus. In the current study, we characterized the impact of AMP-DNM on substrate oxidation patterns, food intake, and body weight gain in obese mice. Eight ob/ob mice treated with 100 mg/(kg d) AMP-DNM mixed in the food and 8 control ob/ob mice were placed in metabolic cages during the first, third, and fifth week of the experiment for measurement of substrate oxidation rates, energy expenditure, activity, and food intake. Mice were killed after 6 weeks of treatment. Initiation of treatment with AMP-DNM resulted in a rapid increase in fat oxidation by 129% (P = .05), a decrease in carbohydrate oxidation by 35% (P = .01), and a reduction in food intake by approximately 26% (P < .01) compared with control mice. Treatment with AMP-DNM decreased hepatic triglyceride content by 66% (P < .01) and, in line with the elevated fat oxidation rates, increased hepatic carnitine palmitoyl transferase 1a expression. Treatment with AMP-DNM increased plasma levels of the appetite-regulating peptide YY compared with control mice. Treatment with AMP-DNM rapidly reduces food intake and increases fat oxidation, resulting in improvement of the obese phenotype. These features of AMP-DNM, together with its insulin-sensitizing capacity, make it an attractive candidate drug for the treatment of obesity and its associated metabolic derangements.

Topics: 1-Deoxynojirimycin; Adamantane; Adipose Tissue; Animals; Body Weight; Carbohydrate Metabolism; Carnitine O-Palmitoyltransferase; Eating; Ghrelin; Glucose; Imino Sugars; Liver; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Oxidation-Reduction; Peptide YY; Triglycerides; Up-Regulation; Weight Gain

Health benefits of resistant starch (RS), a dietary fermentable fiber, have been well documented in young, but not in old populations. As the essential step of more comprehensive evaluations of RS on healthy aging, we examined the effects of dietary RS on tolerance, colonic fermentation, and cytokine expression in aged mice. Healthy older (18-20 months) C57BL/6J male mice were fed control, 18% RS, or 36% RS diets for 10 weeks. Body weight gain, body composition, and fat pad weights did not differ among the three groups after 10 weeks, indicating good tolerance of the RS diet. Fermentation indicators (cecum weights, and cecal proglucagon and PYY mRNA expression) were enhanced in an RS dose-dependent manner (p<0.01). Serum concentrations of soluble cytokine receptors (sTNF-Rb, sIL-4R, sIL-2Rα, sVEGFR1, and sRAGE) and TNFα expression (gene and protein) in visceral fat did not differ significantly among groups. Adiponectin protein concentrations, but not gene expression, were greater in epididymal fat of the 36% RS versus control groups (p<0.05). As a conclusion in aged mice, dietary RS is well tolerated, fermented in the colon, and stimulates colonic expression of proglucagon and PYY mRNA, and adiponectin protein in visceral fat.

Topics: Adiponectin; Aging; Animals; Cecum; Colon; Dietary Fiber; Fermentation; Gene Expression Regulation; Intra-Abdominal Fat; Male; Mice; Mice, Inbred C57BL; Peptide YY; Proglucagon; Receptors, Cytokine; RNA, Messenger; Starch; Tumor Necrosis Factor-alpha; Weight Gain

The objective was to elucidate the relationships between serum concentrations of the gut hormone peptide YY (PYY) and ghrelin and growth development in infants for potential application to the clinical observation index. Serum concentrations of PYY and ghrelin were measured using radioimmunoassay from samples collected at the clinic. For each patient, gestational age, birth weight, time required to return to birth weight, rate of weight gain, time required to achieve recommended daily intake (RDI) standards, time required for full-gastric feeding, duration of hospitalization, and time of administration of total parenteral nutrition were recorded. Serum PYY and ghrelin concentrations were significantly higher in the preterm group (N = 20) than in the full-term group (N = 20; P < 0.01). Within the preterm infant group, the serum concentrations of PYY and ghrelin on postnatal day (PND) 7 (ghrelin = 1485.38 ± 409.24; PYY = 812.37 ± 153.77 ng/L) were significantly higher than on PND 1 (ghrelin = 956.85 ± 223.09; PYY = 545.27 ± 204.51 ng/L) or PND 3 (ghrelin = 1108.44 ± 351.36; PYY = 628.96 ± 235.63 ng/L; P < 0.01). Both serum PYY and ghrelin concentrations were negatively correlated with body weight, and the degree of correlation varied with age. Serum ghrelin concentration correlated negatively with birth weight and positively with the time required to achieve RDI (P < 0.05). In conclusion, serum PYY and ghrelin concentrations reflect a negative energy balance, predict postnatal growth, and enable compensation. Further studies are required to elucidate the precise concentration and roles of PYY and ghrelin in newborns and to determine the usefulness of measuring these hormones in clinical practice.

Topics: Body Weight; Case-Control Studies; Energy Intake; Female; Ghrelin; Humans; Infant, Newborn; Infant, Premature; Male; Nutritional Requirements; Peptide YY; Radioimmunoassay; Weight Gain

Second generation antipsychotics are commonly prescribed for the treatment of schizophrenia, however some can induce metabolic dysfunction side-effects such as weight gain, obesity and diabetes. Clinical reports suggest olanzapine alters satiety signals, although findings appear conflicting. Previous animal model studies have utilised a range of olanzapine dosages, however the dosage that better mimics the human scenario of olanzapine-induced weight gain is unclear. Female Sprague-Dawley rats were treated orally, three times daily with olanzapine (0.25mg/kg, 0.5mg/kg, 1.0mg/kg, 2.0mg/kg), self-administered in a sweet cookie dough pellet at eight-hourly intervals) or vehicle (n=12/group) for 14-days. Olanzapine orally self-administered in multiple doses (eight-hourly intervals) may circumvent a drop in plasma drug concentration and ensure the maintenance of a consistently high olanzapine level in the rat. Olanzapine increased body weight (0.5mg/kg, 1.0mg/kg, 2.0mg/kg), food intake (2.0mg/kg) and feeding efficiency (0.5-2.0mg/kg), with no effect on water intake. Subcutaneous inguinal (1.0mg/kg, 2.0mg/kg) and intra-abdominal perirenal fat were increased (2.0mg/kg), but not interscapula brown adipose tissue. Olanzapine increased circulating ghrelin and cholecystokinin, but had no effect on peptide YY((3-36)). Olanzapine decreased insulin (0.25-2.0mg/kg) and locomotor activity in the open field arena (0.5-2.0mg/kg). A low dosage of 0.25mg/kg olanzapine had no effect on most parameters measured. Olanzapine-induced weight gain is associated with hyperphagia, enhanced feeding efficiency and adiposity, decreased locomotor activity and altered satiety signaling. The animal model used in the present study of self-administered oral olanzapine treatment (t.i.d.) at a dosage range of 0.5-2.0mg/kg (but not 0.25mg/kg) mimics aspects of the clinic.

Topics: Adiposity; Analysis of Variance; Animals; Behavior, Animal; Benzodiazepines; Cholecystokinin; Dose-Response Relationship, Drug; Drug Administration Schedule; Eating; Exploratory Behavior; Female; Hormones; Intra-Abdominal Fat; Metabolic Diseases; Olanzapine; Peptide Fragments; Peptide YY; Rats; Rats, Sprague-Dawley; Selective Serotonin Reuptake Inhibitors; Self Administration; Statistics as Topic; Weight Gain

Peptide YY (PYY) is an endogenous anorectic gut-secreted peptide that has been shown to suppress appetite in animals and humans, when given by injection. This study tested if needle-free pulmonary delivery of PYY enables food intake suppression and reduced body weight gain in rats. The PYY pharmacokinetics and effects on brain neuropeptide levels were also examined.. Rats received single or once-daily 7-day pulmonary administration of saline or PYYs. Food intake and body weight gain were monitored to study the effects of different doses (0.08-0.90 mg/kg) of PYY3-36, PYY1-36 and PYY13-36. Plasma PYY pharmacokinetics were determined via enzyme-linked immunosorbent assay. Changes in orexigenic neuropeptide Y (NPY) and c-Fos protein levels in the hypothalamus arcuate nucleus (ARC) were measured by immunofluorescence microscopy.. PYY3-36 caused dose-dependent and 4- to 6-h food intake suppression following pulmonary delivery. At 0.80 mg/kg, the effect was significant with 35.1 ± 5.7 and 19.7 ± 4.2% suppression at 4 and 6 h, respectively. Repeated administration for 7 days reduced cumulative body weight gain by 39.4 ± 11.0%. PYY1-36, but not PYY13-36, was equipotent to PYY3-36 in food intake suppression. The plasma PYY concentration reached its peak at 10 min following pulmonary delivery with 12-14% of bioavailability. Increased c-Fos and reduced NPY expressions were observed in the hypothalamus ARC, consistent with the magnitude of food intake suppression by each of the PYYs.. Pulmonary delivery of PYY enabled significant 4- to 6-h food intake suppression via 12-14% of lung absorption and hypothalamic ARC interaction, leading to reduced body weight gain in rats.

Topics: Animals; Appetite Regulation; Arcuate Nucleus of Hypothalamus; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Feeding Behavior; Microscopy, Fluorescence; Neuropeptide Y; Peptide Fragments; Peptide YY; Proto-Oncogene Proteins c-fos; Rats; Weight Gain

Resveratrol, a natural polyphenolic compound, was shown to protect rodents against high-fat-diet induced diabesity by boosting energy metabolism. To the best of our knowledge, no data is yet available on the effects of resveratrol in non-human primates. Six non-human heterotherm primates (grey mouse lemurs, Microcebus murinus) were studied during four weeks of dietary supplementation with resveratrol (200 mg/kg/day) during their winter body-mass gain period. Body mass, spontaneous energy intake, resting metabolic rate, spontaneous locomotor activity and daily variations in body temperature were measured. In addition, the plasma levels of several gut hormones involved in satiety control were evaluated.. Resveratrol reduced the seasonal body-mass gain by concomitantly decreasing energy intake by 13% and increasing resting metabolic rate by 29%. Resveratrol supplementation inhibited the depth of daily torpor, an important energy-saving process in this primate. The daily amount of locomotor activity remained unchanged. Except for an increase in the glucose-dependent insulinotropic polypeptide, a gut hormone known to promote mobilization of fat stores, no major change in satiety hormone plasma levels was observed under resveratrol supplementation.. These results suggest that in a non-human primate, resveratrol reduces body-mass gain by increasing satiety and resting metabolic rate, and by inhibiting torpor expression. The measured anorectic gut hormones did not seem to play a major role in these observations.

Topics: Animals; Cheirogaleidae; Energy Intake; Energy Metabolism; Gastric Inhibitory Polypeptide; Glucagon-Like Peptide 1; Male; Motor Activity; Pancreatic Polypeptide; Peptide YY; Resveratrol; Satiety Response; Stilbenes; Weight Gain

The Study of the Effects of Diet on Metabolism and Nutrition (STEDMAN) Project uses comprehensive metabolic profiling to probe biochemical mechanisms of weight loss in humans. Measurements at baseline, 2 and 4 weeks, 6 and 12 months included diet, body composition, metabolic rate, hormones, and 80 intermediary metabolites measured by mass spectrometry. In 27 obese adults in a behavioral weight loss intervention, median weight decreased 13.9 lb over the first 6 months, then reverted towards baseline by 12 months. Insulin resistance (HOMA) was partially ameliorated in the first 6 months and showed sustained improvement at 12 months despite weight regain. Ghrelin increased with weight loss and reverted to baseline, whereas leptin and PYY fell at 6 months and remained persistently low. NPY levels did not change. Factors possibly contributing to sustained improvement in insulin sensitivity despite weight regain include adiponectin (increased by 12 months), IGF-1 (increased during weight loss and continued to increase during weight regain), and visceral fat (fell at 6 months but did not change thereafter). We observed a persistent reduction in free fatty acids, branched chain amino acids, and related metabolites that may contribute to improved insulin action. These findings provide evidence for sustained benefits of weight loss in obese humans and insights into mechanisms.

Topics: Adiponectin; Adult; Behavior Therapy; Biomarkers; Body Weight; Diet; Energy Metabolism; Female; Ghrelin; Humans; Insulin Resistance; Insulin-Like Growth Factor I; Leptin; Middle Aged; Neuropeptide Y; Obesity; Peptide YY; Weight Gain; Weight Loss

Weight gain in women receiving chemotherapy for breast cancer is associated with a higher risk of recurrence but its mechanisms are poorly understood.. To investigate this, we assessed the metabolic, cytokine, and appetite-related peptide alterations during adjuvant chemotherapy for early breast cancer in postmenopausal women, and correlated these with body mass measurements. Specifically, we performed global metabolic profiling using (1)H-nuclear magnetic resonance spectroscopy of sequential sera, examined ghrelin immunoreactivity, RIAs for GLP-1 and peptide YY, and electrochemiluminescent cytokine analyses (tumor necrosis factor-alpha and interleukin-6) on sequential samples.. In those who gained >1.5 kg, several metabolite levels were positively associated with weight gain, specifically lactate, which was 63.5% greater in patients with increased body weight during chemotherapy compared with those with no weight gain (P < 0.01; the prespecified primary end point). A strong correlation (r = 0.7, P < 0.001) was detected between the rate of weight change and serum lactate levels, and on average, lactate levels exhibited the greatest metabolic response to chemotherapy, increasing by up to 75%. Normalized levels of peptide YY were also observed to be elevated in patients not gaining weight posttreatment (+30% compared with -7% for the weight gain group; P < 10(-4)). Baseline lactate, alanine, and body fat were all prognostic for weight gain (area under the receiver operator characteristic curves, >0.77; P < 0.05). No associations were observed between any other parameter and weight gain, including cytokine levels.. Metabonomics identifies excess energy expenditure pathways perturbed during chemotherapy for breast cancer, and establishes a significant association between serum lactate, body fat, and substantive weight gain during chemotherapy.

Topics: Biomarkers; Body Mass Index; Breast Neoplasms; Female; Glucagon-Like Peptide 1; Humans; Interleukin-6; Lactates; Peptide YY; Postmenopause; Tumor Necrosis Factor-alpha; Weight Gain

In humans, ghrelin has been found to stimulate appetite while PYY3-36 to reduce it; these orexigenic and anorexigenic peptides play significant roles in appetite control. We investigated pre- and postprandial responses of ghrelin and PYY in anorexia nervosa (AN) and the influence of weight gain.. Plasma ghrelin, PYY3-36, glucose and insulin responses after ingestion of a 400 kcal standard meal were measured in 14 patients with restricting type of AN and 12 controls. The AN patients were evaluated before therapy and after inpatient therapy. Psychometry was performed by the use of Eating Disorders Inventory.. Ghrelin was suppressed during the meal test, while PYY3-36 was increased in all of the groups. Before therapy, AN patients had significantly increased levels of ghrelin and PYY3-36 compared to the control (P<0.01). After therapeutic intervention, as the nutritional status of AN patients improved, the secretion of these hormones were increased (P<0.05), but not normalized as in psychological testing. In contrast, insulin and glucose responses were normalized after inpatient therapy.. We found that both ghrelin and PYY3-36 increased in AN patients and these changes were not normalized in contrast to insulin after treatment. The increase in both orexigenic ghrelin and anorexigenic PYY3-36 may have a role in pathological eating behavior in AN.

Topics: Adolescent; Adult; Anorexia Nervosa; Appetite; Behavior Therapy; Blood Glucose; Body Composition; Combined Modality Therapy; Eating; Female; Follow-Up Studies; Ghrelin; Humans; Insulin; Nutrition Assessment; Patient Admission; Peptide Fragments; Peptide Hormones; Peptide YY; Postprandial Period; Selective Serotonin Reuptake Inhibitors; Weight Gain

Recent findings suggest that low plasma peptide YY (PYY) levels may contribute to diet-induced human obesity and justify PYY replacement therapy. Although the pharmacological value of PYY is controversial, further study of the secretion of the precursor PYY(1-36) and the pharmacologically active PYY(3-36) is indicated to determine the potential role in energy balance regulation.. Our objective was to determine the effects of acute and chronic changes in human body weight on circulating levels of the putative satiety hormone peptide YY.. Total plasma PYY levels (PYY(1-36) + PYY(3-36)) were measured in 66 lean, 18 anorectic, 63 obese, and 16 morbidly obese humans. In addition, total PYY was measured in 17 of the obese patients after weight loss and in the 18 anorectic patients after weight gain. Fasting PYY(3-36) levels were measured in 17 lean and 15 obese individuals.. Fasting total plasma PYY levels were highest in patients with anorexia nervosa (80.9 +/- 12.9 pg/ml, P < 0.05) compared with lean (52.4 +/- 4.6 pg/ml), obese (43.9 +/- 3.8 pg/ml), or morbidly obese (45.6 +/- 11.2 pg/ml) subjects. In obese patients, weight loss of 5.4% was associated with a 30% decrease in fasting total PYY plasma levels. In anorectic patients, weight gain had no effect on fasting PYY. PYY(3-36) levels did not differ between lean (96.2 +/- 8.6 pg/ml) and obese (91.5 +/- 6.9 pg/ml) subjects.. Our findings do not support a role for abnormal circulating PYY in human obesity. We conclude that circulating PYY levels in humans are significantly elevated in anorexia nervosa and, given the controversially discussed anorectic effect of PYY, could theoretically contribute to that syndrome.

Topics: Adult; Anorexia; Body Weight; Energy Intake; Fasting; Female; Humans; Leptin; Obesity, Morbid; Peptide Fragments; Peptide YY; Receptors, Cell Surface; Receptors, Leptin; Satiety Response; Weight Gain; Weight Loss

Adolescents with anorexia nervosa (AN) have low bone mineral density (BMD). Adipokines and insulin play an important role in bone metabolism in healthy individuals. However, their association with bone metabolism in AN is unknown.. The aim of the study was to determine whether adipokines and insulin are independently associated with measures of BMD in adolescents with AN and controls.. Levels of adiponectin and insulin, fasting and after oral glucose, were evaluated in 17 AN patients and 19 controls (age, 12-18 yr), in whom hormonal parameters [GH, IGF-I, cortisol, estradiol, leptin, ghrelin, and peptide YY (PYY)] had been previously determined. Body composition, bone mineral content, and BMD at the lumbar spine, hip, femoral neck, and total body were assessed by dual energy x-ray absorptiometry. Two bone formation and bone resorption markers were examined.. The study was conducted at a General Clinical Research Center.. Adiponectin differed between AN subjects and controls after controlling for fat mass and decreased in both after oral glucose (P = 0.02 and 0.07). On regression modeling, independent associations were observed of: 1) body mass index and adiponectin with lumbar spine bone mineral apparent density Z-scores (r(2) = 0.45); 2) lean mass, PYY, and ghrelin with hip Z-scores (r(2) = 0.55); 3) adiponectin and lean mass with femoral neck-bone mineral apparent density Z-scores (r(2) = 0.34); and 4) lean mass, PYY, GH, and ghrelin with total body-bone mineral content/height Z-scores (r(2) = 0.64), for the combined group. Adiponectin was also independently associated with BMD, and insulin was associated with bone turnover markers in the groups considered separately.. Adiponectin contributes significantly to the variability of bone density, and insulin contributes to bone turnover markers in adolescent girls.

Topics: Adiponectin; Adolescent; Anorexia Nervosa; Blood Glucose; Body Composition; Bone and Bones; Bone Density; Estradiol; Female; Human Growth Hormone; Humans; Hydrocortisone; Insulin; Insulin Resistance; Insulin-Like Growth Factor I; Peptide YY; Regression Analysis; Weight Gain

Peptide YY(3-36) [PYY(3-36)] is a gut-brain peptide that decreases food intake when administered by intravenous infusion to lean and obese humans and rats. However, chronic administration of PYY(3-36) by osmotic minipump to lean and obese rodents produces only a transient reduction in daily food intake and weight gain. It has recently been shown that 1-h intravenous infusions of PYY(3-36) every other hour for 10 days produced a sustained reduction in daily food intake, body weight, and adiposity in lean rats. Here, we determined whether intermittent delivery of PYY(3-36) can produce a similar response in diet-induced obese rats. During a 21-day period, obese rats (body fat >25%) received twice daily intraperitoneal infusion of vehicle (n = 18) or PYY(3-36) (n = 24) during hours 1-3 and 7-9 of the dark period. Rats had free access to both a 45% fat solid diet and a 29% fat liquid diet; intakes were determined from continuous computer recording of changes in food container weights. To sustain a 15-25% reduction in daily caloric intake, the initial PYY(3-36) dose of 30 pmol.kg(-1).min(-1) was reduced to 10 pmol.kg(-1).min(-1) on day 10 and then increased to 17 pmol.kg(-1).min(-1) on day 13. This dosing strategy produced a sustained reduction in daily caloric intake of 11-32% and prevented body weight gain (8 +/- 6 vs. 51 +/- 11 g) and fat deposition (4.4 +/- 7.6 vs. 41.0 +/- 12.8 g). These results indicate that intermittent intraperitoneal infusion of PYY(3-36) can produce a sustained reduction in food intake and adiposity in diet-induced obese rodents consuming palatable high-fat foods.

Topics: Adiposity; Animals; Body Weight; Diet; Dose-Response Relationship, Drug; Eating; Energy Intake; Infusions, Intravenous; Infusions, Parenteral; Male; Obesity; Peptide Fragments; Peptide YY; Rats; Rats, Sprague-Dawley; Weight Gain

Maternal obesity has been reported as a risk factor for various maternal and fetal complications. The aim of the present study was to examine the patterns of basal and postprandial plasma concentrations of certain gut hormones affecting food intake such as acylated ghrelin, peptide YY(3-36) (PYY(3-36)), cholecystokinin (CCK), insulin and glucose in pregnant women with varying body mass gain during physiological pregnancy. The study included 34 women with singleton pregnancies in the 2(nd) trimester of gestation. The examined pregnant women were divided into 4 groups; I. control pregnancy (CP) with weight gain below 0.5 kg/week; II. overweight low weight gain <1 kg/week (OLWG), III. overweight high weight gain >1 kg/week (OHWG); morbidly obese pregnant with weight gain >1.5 kg/week (MOP). The basal acylated-ghrelin levels in MOP subjects were significantly higher than those in CP and no usual suppression of acylated ghrelin after the meal observed in CP as well as in OLWG and OHWG was found in MOP women. Basal PYY(3-36) plasma levels were similar in CP, OLWG and OHWG but in MOP was significantly reduced and no significant increase in hormone level, typically observed in CP, was detected after a meal in overweight or obese women studied. The fasting CCK and C-reactive protein (CRP) levels in MOP subjects were significantly higher than those in CP and other overweight women. In conclusion, we found that pregnant women with overweight and obesity exhibit significant changes in fasting and postprandial gut hormones affecting food intake such as acylated ghrelin, PYY(3-36) and CCK as well as in CRP and these changes might contribute, at least in part, the development of obesity in pregnancy.

Topics: Acylation; Adult; Appetite; Blood Glucose; Body Mass Index; C-Reactive Protein; Cholecystokinin; Fasting; Female; Gastrins; Gastrointestinal Hormones; Ghrelin; Homeostasis; Humans; Insulin; Obesity; Obesity, Morbid; Peptide Hormones; Peptide YY; Poland; Postprandial Period; Pregnancy; Pregnancy Complications; Weight Gain

Peptide YY (PYY) is a gastrointestinal hormone, localized in enteroendocrine L-cells. Its hydrolyzed form PYY(3-36) is a satiety factor. The aim of this study was to identify if intestinal PYY enteroendocrine cells or content correlate with the diet-induced obese (DIO) or diet-resistant (DR) phenotypes. We also examined intestinal sensitivity to PYY and PYY(3-36) in DIO and DR rats. Animals were maintained on a medium-high fat diet and split into DIO and DR groups based on weight gain. PYY immunoreactive cells were unaltered in DIO intestine and stomach compared to DR rats. PYY content and circulating levels were also unchanged in DIO rats. Intestinal PYY and PYY(3-36) responses were enhanced in fasted rats, and equipotent in both DIO and DR jejunum. We conclude that PYY cell number, tissue content and peripheral sensitivity are maintained in DIO rats. Our data suggests that neither PYY nor PYY(3-36) contribute to the maintenance of either the DIO or DR phenotype, and that peripheral resistance to PYY and PYY(3-36) does not accompany DIO.

Topics: Adipose Tissue; Animals; Body Weight; Diet; Dietary Fats; Eating; Enteroendocrine Cells; Fasting; Feeding Behavior; Male; Obesity; Peptide YY; Rats; Rats, Sprague-Dawley; Weight Gain

Topics: Animals; Eating; Gastric Emptying; Insulin Resistance; Mice; Peptide Fragments; Peptide YY; Rats; Weight Gain

The gut hormone peptide YY 3-36 [PYY (3-36)] has been suggested to posses anorexigenic actions in animals and human adults. However, its circulating concentrations and function have not been studied in neonates. Serum concentrations of PYY (3-36) were determined by RIA (RIA) in 62 healthy preterm infants [mean(SD) gestational age, 32.0(2.1) weeks; postnatal age, 40.9(14.8 d)] and 15 healthy fullterm infants of comparable postnatal age and gender. The correlations between PYY (3-36) levels and anthropometric characteristics, food intake, growth rates and circulating concentrations of total PYY, ghrelin, leptin, insulin and adiponectin were examined. Mean (SD) PYY (3-36) concentrations were higher in preterm [543.7(157.6) ng/L) than full term infants [350.9(114.1) ng/L; p < 0.001) and accounted for 48% and 42% of total PYY basal plasma immunoreactivity in preterm and full term infants, respectively. In multiple regression analysis, PYY (3-36) concentrations correlated negatively with the infants' BMI and positively with serum ghrelin concentrations, but not with caloric intake, weight gain or concentrations of any other hormone studied. In conclusion, PYY (3-36) represents almost half of total PYY immunoreactivity in neonates. It's correlations with ghrelin and BMI suggest a role of this peptide in the regulation of energy homeostasis; however, its specific functions and physiologic significance in neonates remain to be elucidated.

Topics: Adiponectin; Adiposity; Body Mass Index; Energy Intake; Energy Metabolism; Female; Gestational Age; Ghrelin; Homeostasis; Humans; Infant, Newborn; Infant, Premature; Insulin; Leptin; Male; Peptide Fragments; Peptide Hormones; Peptide YY; Radioimmunoassay; Weight Gain

Endogenous peptide YY(3-36) (PYY(3-36)) is associated with postprandial regulation of appetite. We investigated the safety and effectiveness of peripherally administered synthetic human PYY(3-36) for 14 days in New Zealand white rabbits. Weight gain and food consumption were assessed and pharmacokinetics and toxicity characterized.. In all, 24 animals were randomized to one of four intravenous treatment groups - control (0.9% saline) or PYY(3-36) bolus at 4.1, 41.0, or 205 microg/kg/day. Body weight and consumption of fixed food allotment were measured daily. Hematology and serum chemistries were profiled at baseline and Day 15, and pharmacokinetics measured following dose 14. Histopathologic examination of designated tissues and organs in control and PYY(3-36) 205 mug/kg animals was conducted. All animals were subject to clinical and macroscopic observation.. The trend effect of higher dose PYY(3-36) on lower average weight was significant (P = 0.01; Day 14 compared to baseline) and its effect on reduced food consumption was suggested (P = 0.065; number of days < or =75% food eaten, compared with control). Hematology and clinical chemistries were within normal limits pretest and at Day 15. No clinical, macroscopic, histologic, or microscopic changes related to the test article were observed over the course of study.. Lower average weight occurs in rabbits treated once daily with intravenous injection PYY(3-36) (205 microg/kg/day) over 14 days. No clinical or histologic signs of toxicity were observed. Further research is warranted to describe alternate routes of peripheral administration for optimizing weight control.

Topics: Animals; Appetite Depressants; Appetite Regulation; Body Weight; Dose-Response Relationship, Drug; Eating; Female; Infusions, Intravenous; Male; Obesity; Peptide Fragments; Peptide YY; Rabbits; Satiety Response; Weight Gain

The gut hormone peptide YY(3-36) [PYY(3-36)] decreases food intake when administered by intravenous infusion to lean and obese humans and rats. Whether chronic administration of PYY(3-36) produces a sustained reduction in food intake and adiposity is the subject of intense debate. Batterham et al. (R. L. Batterham, M. A. Cowley, C. J. Small, H. Herzog, M. A. Cohen, C. L. Dakin, A. M. Wren, A. E. Brynes, M. J. Low, M. A. Ghatei, R. D. Cone, and S. R. Bloom. Nature 418: 650-654, 2002) first reported that PYY(3-36) reduces food intake and weight gain in rats when injected into the peritoneal cavity twice daily for 7 days. Numerous laboratories have failed to confirm that daily injections of PYY(3-36) decrease body weight. Continuous subcutaneous administration of PYY(3-36) by osmotic minipump has been reported to reduce daily food intake in rodents but only during the first 3-4 days of administration. Here we show the effects of different daily patterns of intravenous infusion of PYY(3-36) on food intake, body weight, and adiposity in rats tethered via infusion swivels to computer-controlled pumps. Measurement of food bowl weight recorded by computer every 20 s permitted daily assessment of the instantaneous effects of PYY(3-36) administration on food intake and meal patterns. One-hour intravenous infusions of PYY(3-36) at 30 pmol x kg(-1) x min(-1) every other hour for 10 days produced a sustained reduction in daily food intake of approximately 20% and decreased body weight and adiposity by 7 and 35%, respectively. Thus dosage pattern is critical for producing a sustained effect of PYY(3-36) on food intake and adiposity.

Topics: Adiposity; Animals; Drug Administration Schedule; Feeding Behavior; Injections, Intravenous; Male; Peptide Fragments; Peptide YY; Rats; Rats, Sprague-Dawley; Weight Gain

The gastrointestinal hormone peptide YY is a potent inhibitor of food intake and is expressed early during differentiation of intestinal and pancreatic endocrine cells. In order to better understand the role of peptide YY in energy homeostasis and development, we created mice with a targeted deletion of the peptide YY gene. All intestinal and pancreatic endocrine cells developed normally in the absence of peptide YY with the exception of pancreatic polypeptide (PP) cells, indicating that peptide YY expression was not required for terminal differentiation. We used recombination-based cell lineage trace to determine if peptide YY cells were progenitors for gastrointestinal endocrine cells. Peptide YY(+) cells gave rise to all L-type enteroendocrine cells and to islet partial differential and PP cells. In the pancreas, approximately 40% of pancreatic alpha and rare beta cells arose from peptide YY(+) cells, suggesting that most beta cells and surprisingly the majority of alpha cells are not descendants of peptide YY(+)/glucagon-positive/insulin-positive cells that appear during early pancreagenesis. Despite the anorectic effects of exogenous peptide YY(3-36) following intraperitoneal administration, mice lacking peptide YY showed normal growth, food intake, energy expenditure, and responsiveness to peptide YY(3-36). These observations suggest that targeted disruption of the peptide YY gene does not perturb terminal endocrine cell differentiation or the control of food intake and energy homeostasis.

Topics: Animals; Cell Differentiation; Cell Lineage; Digestive System; Digestive System Physiological Phenomena; Eating; Endocrine System; Energy Metabolism; Gene Deletion; Gene Expression Regulation, Developmental; Homeostasis; Islets of Langerhans; Mice; Mice, Transgenic; Peptide YY; Transgenes; Weight Gain

Recently peptide YY (PYY) has attracted interest as a possible regulator of food intake. Release of PYY by nutrients in the distal small intestine is thought to contribute to the so-called ileal brake by inhibiting motility and secretion in the foregut. Our objective was to establish whether plasma concentrations of the gut peptides PYY and glucagon-like peptide-1 in rats and humans change in response to intake of a non-absorbable but fermentable carbohydrate.. The acute response was determined in rats by killing animals 0, 5, 10, and 24 h after a single meal with or without lactitol (100 g/kg of semisynthetic diet) and measuring PYY and glucan-like peptide-1 concentrations in plasma. Food intake, body mass, and plasma peptide levels were also determined in rats fed the same diet for 10 d. Healthy human volunteers consumed lactitol or sucrose as a fruit-flavored drink. Breath hydrogen levels were measured at 45-min intervals over the next 7.5 h and plasma peptide concentrations were assessed after 0 and 5 h. Volunteers were also asked to complete a questionnaire to record satiety and well-being.. Ingestion of lactitol significantly increased the acute postprandial PYY response in rats, and prolonged consumption decreased weight gain in growing rats. In humans given a single dose of lactitol, the effects on PYY were much less marked but the postprandial decrease in circulating concentrations of PYY was attenuated. There was no effect on plasma glucan-like peptide-1.. Our observations are consistent with a role for fermentation products in the release of gastrointestinal peptides in the rat and, to a lesser extent, in humans.

Topics: Analysis of Variance; Animals; Breath Tests; Fermentation; Glucagon-Like Peptide 1; Humans; Hydrogen; Male; Peptide YY; Postprandial Period; Rats; Rats, Wistar; Satiety Response; Sugar Alcohols; Weight Gain

Topics: Animals; Appetite; Appetite Depressants; Clinical Trials as Topic; Humans; Peptide Fragments; Peptide YY; Publishing; Rats; Reproducibility of Results; Stress, Physiological; Weight Gain

Parenterally nourished preterm infants commonly receive minimal enteral feedings, the aim being to enhance intestinal function. Whether this regimen increases intestinal growth has not been established.. Our objective was to determine the minimal enteral nutrient intakes necessary to stimulate and to normalize neonatal intestinal growth.. Intestinal growth and cell proliferation were quantified in neonatal pigs given equal amounts of an elemental nutrient solution for 7 d. Different groups (n = 5-7 per group) received 0%, 10%, 20%, 40%, 60%, 80%, or 100% of total nutrient intake enterally, with the remainder given parenterally.. In the jejunum, wet weight, protein mass, and villus height were significantly greater at enteral intakes >40%. Stimulation of ileal protein mass required a higher enteral intake (60%). In both segments, abrupt increases in DNA mass, crypt depth, ornithine decarboxylase activity, and crypt cells in S-phase occurred between enteral intakes of 40% and 60%. Circulating concentrations of glucagon-like peptide-2 and peptide YY, but not gastrin, increased significantly between enteral intakes of 40% and 60% and closely paralleled indexes of cell proliferation.. The minimal enteral nutrient intake necessary to increase mucosal mass was 40% of total nutrient intake, whereas 60% enteral nutrition was necessary to sustain normal mucosal proliferation and growth. Our results imply that providing <40% of the total nutrient intake enterally does not have significant intestinal trophic effects.

Topics: Animals; Animals, Newborn; Cell Division; DNA; Enteral Nutrition; Food, Formulated; Gastrins; Glucagon-Like Peptide 2; Glucagon-Like Peptides; Ileum; Intestines; Jejunum; Nutritional Requirements; Organ Size; Peptide YY; Peptides; Proteins; Swine; Weight Gain

Short day photoperiod promotes thermogenesis and extensive weight loss in Siberian hamsters (Phodopus sungorus sungorus). To determine whether a change in hormone-sensitive lipolysis occurs after short-photoperiod exposure, some lipolytic responses were measured on white adipocytes isolated from animals exposed in warm conditions to short or Long daylight photoperiod. The body mass of male Siberian hamsters exposed during 11 weeks to short days (SD; light: dark, 6:18 hr) reached only 50% of those kept in long days (LD; 16: 8 hr). In SD-hamsters, adipose depot mass also represented approximately 50% of the LD group. A lower DNA content was observed in intra-abdominal fat pads of SD-hamsters. Lipolytic responses to noradrenaline, adrenaline, isoproterenol and ACTH were unchanged. However, sensitivity to the beta-3 adrenergic agonist, BRL 37344, was moderately increased. The major component of the adrenergic control of lipolysis was mediated by beta-3 adrenoceptors in both LD- and SD-Siberian hamsters. The limited antilipolytic effect of alpha-2 adrenergic agonists, PYY or insulin was rather surprising in Siberian hamsters since these inhibitory systems are efficient in hibernants and other photoperiod-sensitive rodents. Our results show that, after short photoperiod exposure, white adipose tissue mass and DNA content are reduced, especially in the epididymal fat pad, with only minor changes in the adipocyte sensitivity to lipolytic hormones.

Topics: Adipocytes; Adipose Tissue; Adrenergic beta-Agonists; Adrenocorticotropic Hormone; Animals; Cricetinae; DNA; Epinephrine; Ethanolamines; Isoproterenol; Lipolysis; Male; Norepinephrine; Peptide YY; Phodopus; Photoperiod; Propanolamines; Sympathomimetics; Weight Gain; Weight Loss