Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bulimia patients claim to crave sweets and since as clinical evidence suggests that the food consumed during eating binges often contains large amounts of carbohydrates, hormones involved in carbohydrate metabolism might be affected in bulimia. We therefore performed a 4-hr glucose tolerance test (GTT), using 100 g oral glucose and inquired about attitudes toward sweets. Thirteen female patients, with a mean age of 23.3 years, who had had bulimia from 3 to 7 years but whose binge-eating/vomiting behavior was largely controlled at the time of testing, were compared to 14 age-matched healthy female controls with a mean age of 24.4 years. All bulimic patients and most controls had liked sweets as children and still liked sweets. Significantly more bulimic patients than controls stated they overate on sweets and avoided sweets. Glucose utilization and the insulin, glucagon, growth hormone (GH), and pancreatic polypeptide (PP) response curves in the bulimic patients were within the normal range. Fasting plasma levels of glucose, insulin, glucagon, GH, cortisol, free fatty acids (FFA), and PP were not different from controls. There was a trend in bulimic patients to have lower plasma FFA levels and higher plasma cortisol levels during the GTT than controls. The findings suggest that, given body weight maintenance and adequate nutrition, patients with bulimia nervosa have normal glucose tolerance and normal hormonal responses following an oral glucose load.
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PMID:Hormone and metabolite plasma levels after oral glucose in bulimia and healthy controls. 304 27

Nineteen bulimic women and 22 age-matched controls were randomly assigned to receive 25 g of glucose or a placebo injection under double-blind conditions. Blood samples of glucose, insulin, and glucagon, and psychometric assessments of mood and food cravings were obtained 10 min before, and 0, 5, 10, 20, 30, 45, and 60 min after injection. Blood levels of the large neutral amino acids (LNAAs) tryptophan, tyrosine, leucine, valine, phenylalanine, and leucine were determined at 10 min before and 60 min after the injection. Bulimic subjects were found to report more symptoms of distressed mood throughout the entire monitoring period than controls. Five minutes following glucose ingestion the self-reports of depression, fatigue, anxiety, and bewilderment rose to a level among the bulimic subjects that was above that at baseline, and was higher than that of bulimia nervosa (BN) subjects receiving placebo. No comparable change in mood was observed among controls. Blood glucose levels were correlated with mood in the bulimic group, but not in controls. In addition, the glucose injection induced a heightened urge to binge in the bulimic group (compared to placebo at 10 and 60 min), whereas reducing food cravings (for sweets) in the controls (at 5 min). When collapsed across time and injection condition, the blood glucose level of bulimics was lower than that of controls. There were no differences in insulin response between the groups. The bulimic group was found to have lower baseline levels of blood tryptophan, whereas no differences in the tryptophan/LNAA ratio were observed either at baseline or following glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind placebo-controlled glucose challenge in bulimia nervosa: psychological effects. 844 64

Binge eating disorder (BED), characterized by ingestion of very large meals without purging afterwards, is found in a subset of obese individuals. We showed previously that stomach capacity is greater in obese than in lean subjects, and in this study, we investigated capacity in obese individuals with BED. We also determined ad-libitum intake of a test meal until extremely full. Furthermore, we measured various appetitive hormones (insulin, leptin, glucagon, CCK, ghrelin) and glucose before a fixed meal and for 120 min afterwards. An acetaminophen tracer was used to assess gastric emptying rate. We compared three groups of overweight women: 11 BED, 13 BE (subthreshold BED), and 13 non-binge-eating normals. The BED individuals had the largest stomach capacity as assessed by either maximum volume tolerated (P=.05) or by gastric compliance to pressure (P=.02) using an intragastric balloon. Although test meal intake did not differ between groups, it correlated (P=.03) with gastric capacity. The BED group showed a tendency (P=.06) to have greater area under the curve (AUC) and had higher values at 5 and 60 min (P<.05) for insulin compared to normals. Moreover, the BED subjects had lower ghrelin baselines premeal, and lower AUC for ghrelin, which then declined less postmeal than for the normals (P<.05). None of the other blood values differed, including glucose, leptin glucagon, and CCK, as well as acetaminophen, reflecting gastric emptying. The lower ghrelin in BED, although contrary to what was expected, is consistent with lower ghrelin in obesity, and suggests down-regulation of ghrelin by overeating. The lack of differences in CCK is consistent with the lack of differences in gastric emptying rate, given that CCK is released when nutrients reach the intestine. The results show that BED subjects have a large gastric capacity as well as abnormalities in meal-related ghrelin and insulin patterns that may be factors in binge eating.
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PMID:Gastric capacity, test meal intake, and appetitive hormones in binge eating disorder. 1523 78

Increased amount of abdominal fat and obesity are common in polycystic ovary syndrome (PCOS). A higher prevalence of bulimia nervosa and greater cravings for sweets have also been reported in these patients. The present study aimed to compare meal-related appetite and secretion of the 'satiety peptide' cholecystokinin (CCK) and glucose regulatory hormones in PCOS women and controls. Sixteen pairs of women with PCOS and controls matched for age and body mass index participated in the study. After an overnight fast, blood samples were collected during ingestion of a standardized meal. We determined basal and postprandial blood levels of CCK, insulin, C-peptide, glucagon, cortisol, growth hormone and glucose. Self-ratings of appetite were assessed by a visual analog scale. PCOS women had a significantly lower meal-related CCK response (p < 0.05) with no association with satiety, as in the controls (r = 0.64). There was a tendency to higher ratings of craving for sweets in PCOS women (p = 0.07) but no correlation with insulin, as in the controls (r = 0.50). Within the PCOS group, ratings of craving for sweets were inversely related to testosterone (r = - 0.60) and the CCK response was positively correlated with levels of free testosterone (r = 0.50). We conclude that women with PCOS have reduced postprandial CCK secretion and deranged appetite regulation associated with increased levels of testosterone. Impaired CCK secretion may play a role in the greater frequency of binge eating and overweight in women with PCOS.
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PMID:Impaired cholecystokinin secretion and disturbed appetite regulation in women with polycystic ovary syndrome. 1562 69

Blood concentrations of the satiety-inducing glucagon-like peptide-1 (GLP-1) were compared in 20 bulimic patients and 20 healthy controls to examine whether secretory impairment of the peptide could be involved in bulimia nervosa (BN). Basal GLP-1 concentrations were measured by means of an enzyme-linked immunosorbent assay (ELISA) in blood samples taken four times over a 12-h period (08.00h, 12.00h, 16.00h, 20.00h) and seven times over a 3-h period following administration of a test meal. Eating-related and non-eating related patients' psychopathological aspects were measured by the use of a battery of ad hoc rating scales (Eating Disorder Inventory-2=EDI-2, Bulimic Investigation test-Edinburgh=B.I.T.E., Montgomery-Asberg Depression Rating Scale=MADRS, Spielberger State-Trait Anxiety Inventory=STAI, Yale-Brown-Cornell Eating Disorder Scale=YBC-EDS). Basal GLP-1 values were higher in patients than in controls only in the blood samples taken at 16.00h, whereas no difference between patients and controls was observed in GLP-1 concentrations in response to the test meal stimulation. GLP-1 levels correlated positively with bingeing-vomiting frequency, with B.I.T.E. scores and the "bulimia" subitem scores of the EDI-2 scale, and negatively with the "ascetism" subitem score of the same scale.
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PMID:Glucagon-like peptide-1 secretion in bulimia nervosa. 1963 91

Lack of control of food intake, excess size, and frequency of meals are critical to the development of obesity. The stomach signals satiation postprandially and may play an important role in control of calorie intake. Sodium alginate (based on brown seaweed Laminaria digitata) is currently marketed as a weight loss supplement, but its effects on gastric motor functions and satiation are unknown. We evaluated effects of 10 days treatment with alginate or placebo on gastric functions, satiation, appetite, and gut hormones associated with satiety in overweight or obese adults. We conducted a randomized, 1:1, placebo-controlled, allocation-concealed study in 48 overweight or obese participants with excluded psychiatric comorbidity and binge eating disorder. All underwent measurements of gastric emptying (GE), fasting, and postprandial gastric volumes (GVs), postprandial satiation, calorie intake at a free choice meal and selected gut hormones after 1 week of alginate (three capsules vs. matching placebo per day, ingested 30 min before the main meal). Six capsules were ingested with water 30 min before the GE, GV, and satiation tests on days 8-10. There were no treatment group effects on GE or volumes, gut hormones (ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY)), satiation, total and macronutrient calorie intake at a free choice meal. There was no difference detected in results between obese and overweight patients. Alginate treatment for a period of 10 days showed no effect on gastric motor functions, satiation, appetite, or gut hormones. These results question the use of short-term alginate treatment for weight loss.
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PMID:Effect of alginate on satiation, appetite, gastric function, and selected gut satiety hormones in overweight and obesity. 2097 79

Binge eating disorder and alcohol use disorder (AUD) frequently co-occur in the presence of other psychiatric conditions. Data suggest that binge eating engages similar behavioral and neurochemical processes common to AUD, which might contribute to the etiology or maintenance of alcoholism. However, it is unclear how binge feeding behavior and alcohol intake interact to promote initiation or maintenance of AUD. We investigated the impact of binge-like feeding on alcohol intake and anxiety-like behavior in male Long Evans rats. Rats received chow (controls) or extended intermittent access (24h twice a week; Int-HFD) to a nutritionally complete high-fat diet for six weeks. Standard rodent chow was available ad-libitum to all groups and food intake was measured. Following HFD exposure, 20.0% ethanol, 2.0% sucrose intake and endocrine peptide levels were evaluated. Anxiety-like behavior was measured using a light-dark (LD) box apparatus. Rats in the Int-HFD group displayed a binge-like pattern of feeding (alternations between caloric overconsumption and voluntary caloric restriction). Surprisingly, alcohol intake was significantly attenuated in the Int-HFD group whereas sugar consumption was unaffected. Plasma acyl-ghrelin levels were significantly elevated in the Int-HFD group, whereas glucagon-like peptide-1 levels did not change. Moreover, rats in the Int-HFD group spent more time in the light side of the LD box compared to controls, indicating that binge-like feeding induced anxiolytic effects. Collectively, these data suggest that intermittent access to HFD attenuates alcohol intake through reducing anxiety-like behavior, a process potentially controlled by elevated plasma ghrelin levels.
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PMID:Intermittent access to a nutritionally complete high-fat diet attenuates alcohol drinking in rats. 2799 22

The worldwide increase in obesity prevalence is a result of positive energy balance, with energy intake exceeding expenditure. The eating behavior in obesity ranges from mild passive overconsumption to excessive overeating with loss of control observed in binge eating disorder (BED). The signaling systems that underlie appetite control in BED are complex and, at this point, not well understood. The present review highlights the current knowledge of key components of the gut peptide system and examines evidence of defects in signaling that differentiate obese binge eaters from obese non-binge eaters. The signaling network underlying hunger, satiety, and metabolic status includes leptin and insulin from energy stores and cholecystokinin, glucagon-like peptide-1, peptide YY(3-36), and ghrelin from the gastrointestinal tract. Of the many gastrointestinal peptides, ghrelin is the only established appetite-stimulating one, whereas cholecystokinin, glucagon-like peptide-1, and peptide YY(3-36) promote satiety. Adipose tissue provides hormonal signals via leptin and insulin to the brain about energy stores and likely from adiponectin and resistin. Binge eating has been related to a dysfunction in the ghrelin signaling system. Moreover, the larger gastric capacity observed in BED may further reduce satiety signals and contribute to overeating.
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PMID:Appetite-Related Gut Peptides in Obesity and Binge Eating Disorder. 2936 37

Binge eating, eating an abnormally large amount of food in a discrete period of time with a sense of loss of control over eating, is a defining feature of the eating disorders binge eating disorder (BED) and bulimia nervosa (BN). Both BED and BN are important public health problems for which there are few medical treatments. However, almost all drugs with central nervous system-mediated weight loss properties studied thus far in randomized, placebo-controlled trials in persons with BED or BN have been efficacious for reducing binge eating behavior. Glucagon-like peptide-1 (GLP-1) receptor agonists, marketed for type 2 diabetes and chronic weight management, produce weight loss in a dose dependent manner and have favorable psychiatric adverse event profiles. We hypothesize that GLP-1 receptor agonists will safely reduce binge eating behavior in individuals with BED or BN, including those with co-occurring psychiatric disorders, and propose that randomized, placebo-controlled clinical trials of GLP-1 receptor agonists be conducted in persons with BED and those with BN. To support this hypothesis, we review studies of GLP-1 and GLP-1 receptor agonists in preclinical models of binge eating, studies of GLP-1 levels in individuals with BED or BN, and preliminary data of GLP-1 receptor agonists in humans with abnormal eating behavior.
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PMID:Would glucagon-like peptide-1 receptor agonists have efficacy in binge eating disorder and bulimia nervosa? A review of the current literature. 2940 5

Recent research indicates that weight suppression (WS: defined as the difference between highest lifetime and current weight) prospectively predicts illness trajectory across eating disorders characterized by binge eating, including AN binge-purge subtype (ANbp), bulimia nervosa (BN), and binge eating disorder (BED), collectively referred to as bulimic eating disorders. Through a series of studies, we have developed a model to explain the link between WS and illness trajectory in bulimic eating disorders. Our model posits that WS contributes to reduced circulating leptin, which leads to reduced postprandial glucagon-like peptide 1 (GLP-1) response. Diminished leptin and GLP-1 function contribute to alterations in two reward-related constructs in the Research Domain Criteria (RDoC): reward value/effort and reward satiation. Respectively, these changes increase drive/motivation to consume food and decrease ability for food consumption to lead to a state of satiation/satisfaction. Combined, these alterations increase risk for experiencing large, out-of-control binge-eating episodes. The following review presents evidence that contributed to the development of this model as well as preliminary findings from an on-going project funded to test this model.
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PMID:Examining weight suppression as a transdiagnostic factor influencing illness trajectory in bulimic eating disorders. 3115 78


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