Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes. Issue 1 (14th October 2015)

• Record Type: Journal Article
• Authors: Zhou, Xinrong; Qian, Bangguo; Ji, Ning; Lui, Conghui; Liu, Zhiyuan; Li, Bing; Zhou, Huarong; Yan, Caifeng
• Is Part Of: Journal of endocrinology. Volume 228:Issue 1(2016)
• Page Start: 13
• Page End: 23
• Publication Date: 2015-10-14
• Subjects: type 2 diabetes mellitus -- gastric bypass surgery -- β-cell -- hyperplasia; Endocrinology -- Periodicals; 616.4005
• DOI: 10.1530/JOE-14-0701
• Languages: English
• ISSNs: 0022-0795

Abstract

Abstract : Gastric bypass surgery produces clear antidiabetic effects in a substantial proportion of morbidly obese patients. In view of the recent trend away from 'bariatric' surgery and toward 'metabolic' surgery, it is important to elucidate the enhancing effect of bypass surgery on pancreatic β-cell mass, which is related to diabetes remission in non-obese patients. We investigated the effects of gastric bypass surgery on glycemic control and other pancreatic changes in a spontaneous non-obese type 2 diabetes Goto-Kakizaki rat model. Significant improvements in postprandial hyperglycemia and plasma c-peptide level were observed when glucose was administered orally post-surgery. Other important events observed after surgery were enhanced first phase insulin secretion in a in site pancreatic perfusion experiment, pancreatic hyperplasia, improved islet structure (revealed by immunohistochemical analysis), striking increase in β-cell mass, slight increase in ratio of β-cell area to total pancreas area, and increased number of small islets closely related to exocrine ducts. No notable changes were observed in ratio of β-cell to non-β endocrine cell area, β-cell apoptosis, or β-cell proliferation. These findings demonstrate that gastric bypass surgery in this rat model increases endocrine cells and pancreatic hyperplasia, and reflect the important role of the gastrointestinal system in regulation of metabolism.