Ernest Adeghate1, Hasan Parvez. 1. Department of Anatomy, Faculty of Medicine and Health Sciences, United Arab Emirates University, PO Box 17666, Al Ain, United Arab Emirates. eadeghate@uaeu.ac.ae
Abstract
OBJECTIVE: Ghrelin is a newly discovered peptide, which was first demonstrated in the epithelium of rat stomach. The purpose of the study was to examine the effect of ghrelin on glucagon secretion from pancreatic tissue fragments of normal and diabetic rats. METHODS: Diabetes was induced by streptozotocin (60 mg Kg body weight 1) given intraperitoneally. Four weeks after the onset of diabetes, pancreatic fragments of normal and diabetic rats were incubated with different concentrations (10 12 10 6 M) of ghrelin. Glucagon release was measured using radioimmunoassay technique. RESULTS: Ghrelin failed to stimulate or inhibit glucagon secretion from normal rat pancreas. However, it induced significant increases in glucagon secretion from pancreatic tissue fragments of diabetic rats. Either atropine (muscarinic cholinergic receptor antagonist) or propranolol (beta-adrenergic receptor antagonist) or yohimbine (alpha2-adrenergic receptor antagonist) or diltiazem (calcium channel antagonist) did not affect ghrelin-glucagon interaction. Moreover, a combination of atropine, propranolol and yohimbine had no significant effect on the interaction of ghrelin with glucagon. CONCLUSION: The ghrelin-induced glucagon secretion in diabetic rats is not controlled via cholinergic or adrenergic pathways. In conclusion, it appears that the main target of ghrelin in the rat endocrine pancreas is not glucagon-producing cells but rather insulin secreting cells which are more involve in weight gain and body growth.
OBJECTIVE:Ghrelin is a newly discovered peptide, which was first demonstrated in the epithelium of rat stomach. The purpose of the study was to examine the effect of ghrelin on glucagon secretion from pancreatic tissue fragments of normal and diabeticrats. METHODS:Diabetes was induced by streptozotocin (60 mg Kg body weight 1) given intraperitoneally. Four weeks after the onset of diabetes, pancreatic fragments of normal and diabeticrats were incubated with different concentrations (10 12 10 6 M) of ghrelin. Glucagon release was measured using radioimmunoassay technique. RESULTS:Ghrelin failed to stimulate or inhibit glucagon secretion from normal rat pancreas. However, it induced significant increases in glucagon secretion from pancreatic tissue fragments of diabeticrats. Either atropine (muscarinic cholinergic receptor antagonist) or propranolol (beta-adrenergic receptor antagonist) or yohimbine (alpha2-adrenergic receptor antagonist) or diltiazem (calcium channel antagonist) did not affect ghrelin-glucagon interaction. Moreover, a combination of atropine, propranolol and yohimbine had no significant effect on the interaction of ghrelin with glucagon. CONCLUSION: The ghrelin-induced glucagon secretion in diabeticrats is not controlled via cholinergic or adrenergic pathways. In conclusion, it appears that the main target of ghrelin in the rat endocrine pancreas is not glucagon-producing cells but rather insulin secreting cells which are more involve in weight gain and body growth.