The Cholinergic System Controls Ghrelin Release and Ghrelin-Induced Growth Hormone Release in Humans

Maier, Christina; Schaller, Georg; Buranyi, B; Nowotny, Peter; Geyer, G; Wolzt, Michael; Luger, Anton

doi:10.1210/jc.2004-0656

Cited by 56 publications

(31 citation statements)

References 33 publications

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“…In humans, plasma ghrelin concentration increased through the activation of the vagal efferent pathway using sham feeding and by a cholinergic agonist such as pyridostigmine [11,36]. On the other hand, plasma ghrelin level was decreased by cholinergic antagonists such as pirenzepine and atropine [36,37]. During acute exercise, vagal efferent activity was attenuated and sympathetic nerve activity increased.…”

Section: Resultsmentioning

confidence: 99%

Significant lowering of plasma ghrelin but not des-acyl ghrelin in response to acute exercise in men

et al. 2011

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Ghrelin, a 28-amino-acid peptide with n-octanoylation indispensable for binding to the growth hormone secretagogue receptor (GHS-R), was originally discovered in the human and rat stomach [1]. Ghrelin molecules are present as two major endogenous forms, an acylated form (ghrelin) and a des-acylated form (desacyl ghrelin). Ghrelin stimulates growth hormone (GH) Abstract. Ghrelin, an acylated peptide produced predominantly in the stomach, stimulates feeding and growth hormone (GH) secretion via interaction with the GH secretagogue receptor. Ghrelin molecules are present in two major endogenous forms, an acylated form (ghrelin) and a des-acylated form (des-acyl ghrelin). Recent studies indicated that aerobic exercise did not change plasma total ghrelin levels, however, dynamics of circulating ghrelin and des-acyl ghrelin during aerobic exercise remains unclear. The purpose of this study is to examine the effects of moderate intensity exercise on plasma ghrelin and des-acyl ghrelin concentrations, and to investigate the relationship between ghrelin molecules and other hormonal and metabolic parameters during exercise. Nine healthy males (25.2 ± 0.5 years) exercised for 60 min at 50% of their maximal oxygen consumptions. We measured the plasma concentrations of ghrelin, des-acyl ghrelin, GH, norepinephrine (NE), epinephrine (E), dopamine (DA), insulin, and glucose. Plasma ghrelin level significantly decreased during exercise, whereas plasma des-acyl ghrelin and total ghrelin levels did not change. Plasma NE, E, DA and GH levels were significantly increased during exercise. Plasma insulin level significantly decreased during exercise, and plasma glucose levels remained steady during exercise. NE, E, DA, and GH were correlated negatively with plasma ghrelin levels. These findings suggest that acute moderate exercise may suppress ghrelin release from the stomach, decrease ghrelin O-acyltransferase activity, and/or activate ghrelin utilization in peripheral tissues and that exercise-induced ghrelin suppression may be mediated by activated adrenergic system.

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Section: Resultsmentioning

confidence: 99%

Significant lowering of plasma ghrelin but not des-acyl ghrelin in response to acute exercise in men

et al. 2011

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“…In vagotomized rats, baseline ghrelin levels and suppression of ghrelin levels by nutrient load were unaltered, but an increase of ghrelin levels induced by 48-h food deprivation was abolished completely, and this result was mimicked by treatment with the unspecific cholinergic antagonist atropine (25). In a group of young healthy human volunteers, atropine promptly and significantly decreased ghrelin plasma concentrations after an overnight fast (26).…”

Section: Conclusion-mentioning

confidence: 92%

Cholinergic Regulation of Ghrelin and Peptide YY Release May Be Impaired in Obesity

Maier

Riedl²,

Vila³

et al. 2008

Diabetes

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1OBJECTIVE-Ghrelin and peptide YY (PYY) are both hormones derived from the gastrointestinal tract involved in appetite regulation. The cholinergic part of the vagal nerve is involved in the regulation of glucose and insulin. The aim of this study was to examine the effects of the cholinergic antagonist atropine on ghrelin, PYY, glucose, and insulin under basal conditions and after meal ingestion in lean and obese subjects.REASEARCH DESIGN AND METHODS-Eight lean and eight obese subjects were included in a randomized, double-blind, placebo-controlled crossover study with 4 study days in randomized order (atropine/placebo Ϯ breakfast). Plasma ghrelin, PYY, insulin, and glucose were measured. Hunger and satiety feelings were rated on a 10-cm visual analog scale. RESULTS-In lean individuals, atropine led to a decrease in ghrelin concentrations comparable and nonadditive with breakfast ingestion and a significant decrease in both basal and meal-induced PYY concentrations. In obese subjects, atropine did not significantly change ghrelin or PYY concentrations, whereas it induced a comparable increase in heart rate and meal-induced glucose concentrations in the two study groups. Only lean, not obese, subjects experienced sustained feelings of satiety after breakfast. CONCLUSIONS-The impaired cholinergic regulation of the postprandial drop in ghrelin concentrations and rise in PYY concentrations might be part of the deregulated food intake in obese subjects.

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“…22 Subsequently, another study reported increased ghrelin levels in subjects undergoing active weight loss after gastric bypass, but not in weight-stable subjects. 23 One explanation for these divergent results could be that surgical techniques may affect the vagus nerve differently, as suggested in an editorial by Cummings and Shannon, 24 as studies in rodents 25 and humans 26,27 have shown that the vagus nerve is essential for ghrelin release.…”

Section: Introductionmentioning

confidence: 99%

Meal suppression of circulating ghrelin is normalized in obese individuals following gastric bypass surgery

et al. 2006

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Objective: It has been proposed that the success of maintained weight loss in morbidly obese subjects following Roux-en-Y gastric bypass (RYGBP) surgery depends on inappropriately low circulating concentrations of the appetite-stimulating peptide ghrelin, being unresponsive to food intake. In this study, this hypothesis was examined. Design: Cross-sectional study with repeated blood samples in 40 subjects after 14 h of prolonged overnight fasting followed by a standardized mixed meal (770 kcal). Subjects: Twenty men and 20 women were included: 10 middle-aged morbidly obese (body mass index (BMI) 43.973.3 kg/ m 2 ), 10 middle-aged subjects who had undergone RYGBP at the Uppsala University Hospital (BMI 34.775.8 kg/m 2 ), 10 middleaged non-obese (BMI 23.572.2 kg/m 2 ) and 10 young non-obese (BMI 22.771.8 kg/m 2 ). Measurements: Ghrelin, glucose and insulin levels were analysed pre-and postprandially. Results: In the morbidly obese, ghrelin concentrations were lower in the morning than in the RYGBP group and did not change following the meal. In the RYGBP group, fasting ghrelin levels fell after meal intake and showed similar suppression as both agematched and young non-obese controls. The RYGBP surgery resulted in an increased meal-induced insulin secretion, which was related to the degree of postprandial ghrelin suppression. Conclusion: The present study demonstrates low circulating concentrations of ghrelin and blunted responses to fast and feeding in morbidly obese subjects. Marked weight reduction after RYGBP at our hospital is followed by a normalization of ghrelin secretion, illustrated by increased fasting levels compared to the preoperative obese state and regain of meal-induced ghrelin suppression.

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The Cholinergic System Controls Ghrelin Release and Ghrelin-Induced Growth Hormone Release in Humans

Cited by 56 publications

References 33 publications

Significant lowering of plasma ghrelin but not des-acyl ghrelin in response to acute exercise in men

Significant lowering of plasma ghrelin but not des-acyl ghrelin in response to acute exercise in men

Cholinergic Regulation of Ghrelin and Peptide YY Release May Be Impaired in Obesity

Meal suppression of circulating ghrelin is normalized in obese individuals following gastric bypass surgery

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