Ghrelin and Feedback Systems

研究成果: Chapter

26 被引用数 (Scopus)

抄録

Ghrelin is produced primarily in the stomach in response to hunger, and circulates in the blood. Plasma ghrelin levels increase during fasting and decrease after ingesting glucose and lipid, but not protein. The efferent vagus nerve contributes to the fasting-induced increase in ghrelin secretion. Ghrelin secreted by the stomach stimulates the afferent vagus nerve and promotes food intake. Ghrelin also stimulates pituitary gland secretion of growth hormone (GH) via the afferent vagus nerve. GH inhibits stomach ghrelin secretion. These findings indicate that the vagal circuit between the central nervous system and stomach has a crucial role in regulating plasma ghrelin levels. Moreover, body mass index modulates plasma ghrelin levels. In a lean state and anorexia nervosa, plasma ghrelin levels are increased, whereas in obesity, except in Prader-Willi syndrome, plasma ghrelin levels are decreased and the feeding- and sleeping-induced decline in plasma ghrelin levels is disrupted. There are two forms of ghrelin: active n-octanoyl-modified ghrelin and des-acyl ghrelin. Fasting increases both ghrelin types compared with the fed state. Hyperphagia and obesity are likely to decrease plasma des-acyl ghrelin, but not n-octanoyl-modified ghrelin levels. Hypothalamic serum and glucocorticoid-inducible kinase-1 and serotonin 5-HT2C/1B receptor gene expression levels are likely to be proportional to plasma des-acyl ghrelin levels during fasting, whereas they are likely to be inversely proportional to plasma desacyl ghrelin levels in an increased energy storage state such as obesity. Thus, a dysfunction of the ghrelin feedback systems might contribute to the pathophysiology of obesity and eating disorders.

本文言語English
ホスト出版物のタイトルGhrelin
編集者Gerald Litwack
ページ149-170
ページ数22
DOI
出版ステータスPublished - 2007

出版物シリーズ

名前Vitamins and Hormones
77
ISSN(印刷版)0083-6729

ASJC Scopus subject areas

  • 生理学
  • 内分泌学

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