Adiponectin Downregulates Hyperglycemia and Reduces Pancreatic Islet Apoptosis After Roux-En-Y Gastric Bypass Surgery

Abstract

The resolution of type 2 diabetes mellitus is an additional outcome of Roux-en-Y gastric bypass (RYGB) surgery. The general objective was to explore whether RYGB could reduce beta cells apoptosis and what roles adiponectin played in downregulating hyperglycemia after RYGB. Twenty Goto-Kakizaki (GK) rats were allocated in RYGB group (ten) and GK group (ten), and ten Wistar (WS) rats were allocated in WS group. RYGB was performed in RYGB group and sham operation in the GK and WS groups. Fasting plasma glucose, body weight, food intake per 100g body weight, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), C peptide, and adiponectin were measured pre- and postoperatively. Terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end-labeling and transmission electron microscopy were performed to detect apoptosis of pancreatic beta cells. Data were analyzed by analysis of variance, Student t test, and post hoc comparisons (Tukey's test). Animals in WS group had significant higher postprandial insulin, C peptide, and adiponectin concentrations compared to RYGB and GK groups preoperatively. Body weight and food intake in RYGB group significantly decreased compared to WS and GK groups postoperatively. Postprandial insulin, C peptide, and adiponectin concentrations significantly increased, while fasting plasma glucose and HOMA-IR values decreased in RYGB group compared to GK group postoperatively. More apoptotic beta cells were detected in GK group than RYGB and WS groups postoperatively. RYGB could increase postprandial insulin and reduce pancreatic islet apoptosis. Adiponectin played a key role in regulating plasma glucose and reducing pancreatic islet apoptosis after RYGB.