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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ghrelin, a gut-brain peptide that signals hunger, is normally suppressed after meals. Subnormal suppression of postprandial ghrelin, previously noted in obese, insulin-resistant individuals, may contribute to increased food intake. Given the ethnic disparities in obesity and obesity-related cardiovascular morbidity in the United States, the present study compared a single postprandial ghrelin measure in 43 women (22 white, 21 black). Each completed a rigorously controlled 4-d dietary intervention designed to maintain weight and constant daily sodium and potassium intake (220 mEq Na, 40 mEq K). Two hours after consuming a test meal of identical content, blood samples were drawn to assess postprandial ghrelin, leptin, and norepinephrine; resting cardiovascular function was measured; and a 24-h urinary cortisol sample was obtained. Independent of body mass index, postprandial ghrelin was significantly higher in black vs. white women, and higher ghrelin was associated with higher cortisol in blacks, who failed to show the expected inverse relation between ghrelin and central obesity seen in whites. Higher ghrelin was correlated with higher blood pressure but lower norepinephrine in obese women. These findings suggest subnormal postprandial ghrelin suppression (or faster ghrelin rebound) in black women, especially the obese, that might play a role in their increased prevalence of obesity and cardiovascular disorders.
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PMID:Postprandial ghrelin is elevated in black compared with white women. 1535 47

Ghrelin, a brain-gut peptide discovered from the stomach, stimulates growth hormone release, food intake, adiposity, and weight gain. Circulating ghrelin levels are modulated under conditions of positive and negative energy balance, however its effect on macronutrient selection is not known. The present experiment investigates the effect of ghrelin on single and two-diet feeding paradigms in high-carbohydrate (HC) and high-fat (HF) preferring rats. In the macronutrient selection test in which rats were given free access to either high-carbohydrate or high-fat diet, an intracerebroventricular (i.c.v.) administration of ghrelin potently enhanced fat intake over carbohydrate intake in both HC- and HF-preferring rats. In the diet preference test in which rats were given free access to both high-carbohydrate and high-fat diets simultaneously, an i.c.v. administration of ghrelin also preferentially enhanced fat consumption over carbohydrate in both HF- and HC-preferring rats. Intracerebroventricular administrations of galanin and neuropeptide Y enhanced fat and carbohydrate ingestion, respectively. Centrally administered ghrelin enhanced fat ingestion. These results provide further insights for the role of ghrelin in feeding behavior and the development of obesity.
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PMID:Central administration of ghrelin preferentially enhances fat ingestion. 1538 Mar 11

Ghrelin, the endogenous ligand for GHS-R, was isolated from rat stomach, although other tissues exist expressing ghrelin, such as pituitary, hypothalamus, placent, ovary, testes, etc. It was showed that ghrelin is implicated in GH secretion, in vivo and in vitro. There are direct evidences that proof that ghrelin administration induces GH secretion. There are in vivo data, showing ghrelin as a most potent GH secretor than GHRH. Evidences exist of ghrelin actions in the regulation of food intake and energy homeostasis. Ghrelin has a clear role in the differents pathologies such as obesity, anorexia and bulimia.
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PMID:[Role of ghrelin in the pathophysiology of eating behaviour]. 1538 8

Obesity is associated with different disturbances in endocrine function. Both spontaneous growth hormone (GH) secretion and its response to several stimuli have shown to be reduced in obese patients. The GH responses to GH-releasing hormone and other challenges by pyridostigmine suggest that the reduction in GH secretion is related to an increased somatostatinergic tone. Other experiments point to a down-regulation of somatostatin receptors in the somatotroph cell. Ghrelin administration is followed by a massive GH release, but the possibility that ghrelin or GHRH deficiency are the cause of GH deficiency in obesity is unlikely. The increase in free fatty acids in obesity might be related to GH reduction, since acipimox administration is able to reverse GH secretion. In women, abdominal obesity is associated with hyperandrogenism and low sex hormone-binding globulin levels. Obese men have low testosterone and gonadotrophin concentrations, specially in cases of morbid obesity. An increase in hypothalamic-pituitary-adrenal axis activity and some resistance to dexamethasone suppression have been described in abdominal obesity. This effect may be due to neuroendocrine alterations related to a genetic origin. Adrenal hyperfunction may favour cardiovascular and metabolic complications. There are no disturbances in thyroid function. Sometimes a reduction in prolactin response to several stimuli has been reported. This effect may be due to hyperinsulinaemia or to disturbances in the dopaminergic tone.
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PMID:[Neuroendocrine disturbances in obesity]. 1538 10

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and alpha-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.
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PMID:Peripheral and central signals in the control of eating in normal, obese and binge-eating human subjects. 1538 23

Anorexia-associated malnutrition is a severe complication that increases mortality in peritoneal dialysis (PD) patients. Ghrelin is a recently-discovered orexigenic hormone with actions in brain and stomach. We analyzed, in 42 PD patients, the possible relationship between ghrelin and appetite regulation with regard to other orexigens [neuropeptide Y (NPY), NO3] and anorexigens [cholecystokinin (CCK), leptin, glucose-dependent insulinotropic peptide (GIP), tumor necrosis factor alpha (TNFalpha)]. All orexigens and anorexigens were determined in plasma. Eating motivation was evaluated using a visual analog scale (VAS). The patients were divided into three groups: those with anorexia (n = 12), those with obesity associated with high intake (n = 12), and those with no eating behavior disorders (n = 18). A control group of 10 healthy volunteers was also evaluated. Mean plasma levels of ghrelin were high (3618.6 +/- 1533 mg/mL), with 36 patients showing values above the normal range (< 2600 mg/mL). Patients with anorexia had lower ghrelin and NPY levels and higher peptide-C, CCK, interleukin-1 (IL-1), TNFalpha, and GIP levels than did the other patients. Patients with anorexia also had an early satiety score and low desire and pleasure in eating on the VAS and diet survey. We observed significant positive linear correlations between ghrelin and albumin (r = 0.43, p < 0.05), prealbumin (r = 0.51, p < 0.05), transferrin (r = 0.4, p < 0.05), growth hormone (r = 0.66, p < 0.01), NO3 (r = 0.36, p < 0.05), and eating motivation (VAS). At the same time, negative relationships were observed between blood ghrelin and GIP (r = -0.42, p < 0.05), insulin (r = -0.4, p < 0.05), leptin (r = -0.45, p < 0.05), and creatinine clearance [r = -0.33, p = 0.08 (nonsignificant)]. Ghrelin levels were not related to Kt/V or to levels of CCK and cytokines. Ghrelin plasma levels are elevated in PD patients. Uremic patients with anorexia show relatively lower ghrelin plasma levels than the levels seen in obese patients or in patients with normal appetite. The role of ghrelin in appetite modulation is altered in uremic PD patients, and that alteration is possibly associated with disorders in insulin and growth hormone metabolism.
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PMID:Ghrelin plasma levels and appetite in peritoneal dialysis patients. 1538 25

Ghrelin is a member of the group of growth hormone secretagogues (GHSs). It is a peptide hormone, recently isolated from stomach as an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Ghrelin is mostly produced by the stomach, although its production has been proved in various tissues. It is a potent releaser of growth hormone (GH) from anterior pituitary cells, but it also stimulates the release of other hypophyseal hormones. Ghrelin stimulates food intake and induces metabolic changes leading to an increase in body weight and body fat mass. This effect seems to be independent of GH action and needs an intact NPY/AGRP (neuropeptide Y/agouti-related protein) system. Plasma ghrelin levels are decreased in obesity, elevated in cachexia and show a diurnal rhythm. Its preprandial elevation suggests, that it might be a signal for meal initiation. Ghrelin further stimulates the release of gastric acid and gastric motility and affects pancreatic functions. It has vasodilatatory, cardioprotective and antiproliferative effects. This article is focused on ghrelin's endocrine and metabolic functions.
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PMID:Endocrine and metabolic activities of a recently isolated peptide hormone ghrelin, an endogenous ligand of the growth hormone secretagogue receptor. 1549 31

Ghrelin is a peripheral gastric peptide involved in the regulation of eating behavior and energy homeostasis. While changes in ghrelin plasma levels have been found in anorexia nervosa, bulimia nervosa (BN) and obesity, no study has assessed circulating ghrelin in binge eating disorder (BED). Therefore, we measured plasma levels of this peptide in women with BED as compared to women with BN, obesity and healthy controls. One hundred and eighty-two drug-free women (56 bulimics, 13 non-obese and 34 obese BED subjects, 28 obese non-binge eating women and 51 non-obese healthy women) underwent psychopathological and nutritional assessments and blood sample collection for glucose and ghrelin assays in the morning. As compared to non-obese healthy women, both non-obese and obese BED women as well as obese non-binge eating women had significantly increased values of body weight, body mass index and body fat mass. Moreover, plasma ghrelin concentrations were significantly decreased in both non-obese (P<0.01) and obese (P<0.0001) BED women as well as in obese non-binge eating women (P<0.001) but not in women with BN. No significant correlations emerged between plasma ghrelin values and the frequency of binge/vomiting in BN subjects or the frequency of bingeing in BED individuals. The reduction of plasma ghrelin in non-obese and obese binge eaters as well as in obese non-binge eaters may represent a secondary change aiming to counteract their positive energy imbalance.
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PMID:Circulating ghrelin is decreased in non-obese and obese women with binge eating disorder as well as in obese non-binge eating women, but not in patients with bulimia nervosa. 1551 98

Circulating levels of the gastric hormone ghrelin rise before and decrease after a meal. In normal-weight subjects, postprandial suppression of ghrelin is proportional to calories consumed. Obese individuals have lower fasting ghrelin levels; however, it is unclear whether the obese show normal postprandial suppression. This study aimed to compare postprandial ghrelin responses in normal-weight and obese subjects, using mixed macronutrient meals with varied fat and calorie content. Postprandial ghrelin response was measured in normal-weight insulin-sensitive subjects and obese insulin-resistant subjects, after six test meals with different fat and calorie content (250-3000 kcal). Increasing the calorie content of meals in normal-weight subjects progressively lowered nadir levels of ghrelin. The obese had lower fasting ghrelin levels, and the reduction after the consumption of all test meals was less than the normal-weight subjects. The lowest postprandial levels in the obese were no different to the nadir in normal-weight volunteers after 1000-, 2000-, and 3000-kcal meals. Thus, circulating ghrelin levels decreased in normal-weight subjects after mixed meals. Obese subjects demonstrated a much reduced ghrelin postprandial suppression. This reduced suppression may influence satiety, thus reinforcing obesity.
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PMID:Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects. 1552 35

Administration of ghrelin, the endogenous ligand for the GH secretagogue receptor, stimulates not only GH secretion but also appetite and food intake in humans. Endogenous ghrelin levels display a distinct circadian rhythm, which is reciprocal to that of insulin and presumed to be meal dependent and not associated with GH secretion. We tested the hypothesis that food deprivation could impact circadian serum ghrelin levels and unmask meal-independent regulatory mechanisms. Thirty-three young adults, subdivided according to gender and level of obesity, were studied with blood sampling every 3 h from 12-84 h of fasting. Serum ghrelin levels showed a marked diurnal rhythm with a nadir in the morning (0800 h), peak levels in the afternoon, and a gradual decline during the night. This pattern was preserved during the entire fasting period and was independent of gender and obesity. Mean 24-h ghrelin levels exhibited a small but significant decline during the fast (P < 0.001). As expected, GH secretion increased with fasting in lean subjects, and a gradual decline in insulin concentrations was observed in all subjects. Neither GH nor insulin showed any significant relationship to ghrelin. In contrast, serum cortisol exhibited a strong inverse temporal association with ghrelin (r = -0.79; P < 0.0001). In conclusion, our study yields no evidence that ghrelin stimulates GH release during fasting. As a novel finding, ghrelin appears to be related to cortisol. However, further studies are needed to elucidate the physiological mechanisms behind this relationship.
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PMID:Fasting unmasks a strong inverse association between ghrelin and cortisol in serum: studies in obese and normal-weight subjects. 1552 42


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