Effect of Incretins upon B-Cell Autophagy and Apoptosis Induced by a Fructose-Rich Diet

ROMAN CL; BOGGIO V; MAIZTEGUI B; FLORES L; DEL ZOTTO H; ROPOLO A; GRASSO D; CATRINACIO C; VACCARO MI; GAGLIARDINO JJ

San Francisco

Congreso; 74th Scientific Sessions American Diabetes Association (ADA); 2014

American Diabetes Association

Fructose (F) administration to normal rats induces plurimetabolic changes and decreases β-cell mass due to an increased apoptotic rate. Autophagy, a catabolic mechanism that involves cell degradation of dysfunctional organelles, is strongly associated with apoptosis. This process can be involved in the mechanism by which the F-rich diet decreases β-cell mass. Thus, our aim was to determine whether incretins prevent F-induced β-cell autophagy and apoptosis. Normal male Wistar rats were fed (3 weeks) a standard commercial diet (C) or this diet with 10% F in drinking water (F). C and F rats received exendin-4 (0.70 nmol/kg/day; CE and FE) or sitagliptin (115 mg/rat/day; CS and FS). At sacrifice we measured glucose (G), triglyceride (T), fructosamine (Fn) and insulin (I) plasma concentrations, performed an oral G tolerance test (OGTT), and light and electron microscopy and morphometric studies of the endocrine pancreas. Islet LC3 protein expression (immunocytochemistry) was also studied. Results are expressed as % of increase/decrease with respect to C; p