Insulin secretory defect plays a major role in the development of diabetes in patients with distal pancreatectomy

Abstract

To investigate the pathogenesis of distal pancreatectomy (d-Px)–induced diabetes in Korean patients, we investigated insulin secretory and sensitivity indexes obtained by oral glucose tolerance testing in 20 patients that had received d-Px (10 with d-Px–induced diabetes and 10 with normal glucose tolerance with d-Px [NGT d-Px]) and in 164 control subjects (77 with type 2 diabetes mellitus and 87 with NGT) that did not receive d-Px. The pancreatectomized subjects had lower fasting serum insulin, homeostasis model assessment of pancreatic beta-cell function (HOMA- β) levels, and insulinogenic indices than the NGT controls. The HOMA- β values of nonobese NGT d-Px– and d-Px–induced diabetic subjects were 73.7% and 38.7% of those for nonobese NGT controls, respectively, and HOMA- β was significantly lower only for d-Px–induced diabetic subjects ( P < .01). In obese subjects, the HOMA- β values of obese d-Px–induced diabetic subjects were significantly lower than those of obese NGT controls ( P < .05). The insulin sensitivity was significantly lower in nonobese type 2 diabetes mellitus controls than in nonobese NGT d-Px or in nonobese d-Px–induced diabetic subjects ( P < .001 and .05, respectively). These results show that a reduced insulin secretory function is a typical feature of glucose homeostasis in distal pancreatectomized patients and that insulin secretory defect plays a major role in the development of diabetes in these patients. In addition, the study suggests that pancreatic resections of 60% or less and body mass index are not the main causes of diabetes onset after d-Px in this study.