title: Reduced ghrelin production induced anorexia after rat gastric ischemia and reperfusion.
abstract: The gastrointestinal (GI) tract is one of the most susceptible organs to ischemia. We previously reported altered gastric motility after gastric ischemia and reperfusion (I/R). However, there have also been few reports of alterations in the eating behavior after gastric I/R. Ghrelin is a GI peptide that stimulates food intake and GI motility. Although ghrelin itself has been demonstrated to attenuate the mucosal injuries induced by gastric I/R, the endogenous ghrelin dynamics after I/R has not yet been elucidated. The present study was designed to investigate the relationship between food intake and the ghrelin dynamics after gastric I/R. Wistar rats were exposed to 80-min gastric ischemia, followed by 12-h or 48-h reperfusion. The food intake, plasma ghrelin levels, gastric preproghrelin mRNA expression levels, and the histological localization of ghrelin-immunoreactive cells were evaluated. The effect of exogenous ghrelin on the food intake after I/R was also examined. Food intake, the plasma ghrelin levels, the count of ghrelin-immunoreactive cells corrected by the percentage areas of the remaining mucosa, and the expression levels of preproghrelin mRNA in the stomach were significantly reduced at 12 h and 48 h after I/R compared with the levels in the sham-operated rats. Intraperitoneal administration of ghrelin significantly reversed the decrease of food intake after I/R. These data show that gastric I/R evoked anorexia with decreased plasma ghrelin levels and ghrelin production, which appears to be attributable to the I/R-induced gastric mucosal injuries. The decrease in the plasma ghrelin levels may have been responsible for the decreased food intake after gastric I/R.
authors: Div. of Gastroenterology and Hepatology, Dept. of Internal Medicine, Keio Univ. School of Medicine, Tokyo, Japan.
authors: Sachiko
authors: S
authors: Mogami
authors: Hidekazu
authors: H
authors: Suzuki
authors: Seiichiro
authors: S
authors: Fukuhara
authors: Juntaro
authors: J
authors: Matsuzaki
authors: Kenji
authors: K
authors: Kangawa
authors: Toshifumi
authors: T
authors: Hibi
mesh_terms: D000818:Animals; D000855:Anorexia / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D004435:Eating / Q000187:drug effects / Q000502:physiology; D005215:Fasting / Q000097:blood / Q000502:physiology; D005746:Gastric Emptying / Q000502:physiology; D005748:Gastric Fundus / Q000378:metabolism / Q000473:pathology; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D015870:Gene Expression / Q000235:genetics; D054439:Ghrelin / Q000097:blood / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000150:complications* / Q000473:pathology / Q000503:physiopathology
chemical_list: D054439:Ghrelin; C422650:ghrelin, des-n-octanoyl