Taurine supplementation regulates pancreatic islet function in response to potentiating agents in leptin-deficient obese mice.

Abstract

An imbalance of the autonomic nervous system (ANS) is suggested to be involved in insulin hypersecretion in obesity. Taurine (Tau) shows anti-obesity effects and regulates pancreatic islet function. Here, we evaluated obesity development and insulin secretion in response to cholinergic/protein kinase (PK)-C and PKA activation in ob/ob mice supplemented with Tau. From weaning until 90 days of age, male and female C57Bl/6 (C) and ob/ob mice (ob) were supplemented (CT and obT), or not, with 5 % Tau. Female and male ob mice presented higher body weight and fat stores. Tau did not alter adiposity in the obT groups. Islets isolated from female and male ob mice hypersecreted insulin in response to 5.6 and 11.1 mM glucose without or with 100 μM Cch (carbachol), 100 nM PMA (phorbol-12-myristate-13-acetate) or 10 μM forskolin. Additionally, Cch-induced higher intracellular Ca2+ mobilization in ob islets. Islets from the female ob group were not responsive to the inhibitory action of phenylephrine (Phe). Tau decreased insulin release at 5.6 mM glucose without or with PMA in obT. At 11.1 mM glucose, the female obT group presented normal insulin secretion at Cch, PMA and Phe, whereas male obT partially decreased secretion following PMA and forskolin stimuli. Ca2+ mobilization induced by Cch is partially reduced in female obT. Therefore, ob islets presented hypersecretion in glucose and potentiating agents. Despite not preventing the development of obesity, the normalization of the cholinergic/PKC pathway and the improvement in the action of Phe, indicate that Tau may regulate the ANS actions upon endocrine pancreas in obesity.