Introduction: Exenatide (EXE) is an agonist of glucagon-like peptide type 1 receptor. The aim of this study was to evaluate changes in pivotal metabolic parameters under the effect of EXE in rats with obesity induced by L-glutamic acid monosodium salt (MSG). Design and Methods: 24 h after birth, male Wistar rats received a daily subcutaneous (sc) MSG (4 mg/g) (iMSG) or were maintained without treatment (iC) until they were 10 days old. On the 90^th day, obese animals were selected from iMSG group by Lee index>0.3 and subdivided into 2 groups: untreated (OBS) and treated with EXE (10 µg/kg, daily sc) for 20 days (OBSE). Healthy control animals (C) were selected from iC group by Lee index≤0.3. Subsequently, individual blood samples were withdrawn under anesthesia and the animals were then killed by decapitation. Whole retroperitoneal (R) and periepididymal (P) fatty deposits were quickly removed by laparotomy, and their wet mass determined. The evolution of body mass (BM) and naso-anal length (NAL) was monitored throughout treatment. The pancreas was dissected and Langerhans islets (LI) were isolated. Blood glucose (BG) and plasma triglycerides (TG), cholesterol (VLDL, HDL and total), osmolality and total protein, as well the number of LI were measured after a 3 h fasting period. Results: BM: C>OBS=OBSE; NAL: C>OBS=OBSE; Lee index: C<OBS=OBSE; Wet mass of R and P: C<OBS=OBSE; Number of LI: C>OBS, C>OBSE, OBSE>OBS; BG: OBS>C=OBSE; HDL: OBSE>C, C=OBS, OBS=OBSE; TG and VLDL: C<OBS=OBSE; Osmolality, total cholesterol and protein did not differ among all groups. Conclusion: Effect of EXE on HDL was controversial, but its effectiveness to restore glycemia and to increase the number of pancreatic islets together with its ineffectiveness to reduce body mass and adiposity in rats with “central” obesity were evidenced in the present study. 

Supported by: FAPESP, CNPq and CAPES