These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Roux-en-Y gastric bypass-induced improvement of glucose tolerance and insulin resistance in type 2 diabetic rats are mediated by glucagon-like peptide-1. Author: Liu Y, Zhou Y, Wang Y, Geng D, Liu J. Journal: Obes Surg; 2011 Sep; 21(9):1424-31. PubMed ID: 21479766. Abstract: BACKGROUND: The aim of this study was to investigate the effects of Roux-en-Y gastric bypass (RYGB) on glucose tolerance and insulin resistance in type 2 diabetic rats and the possible mechanisms involved in this process. METHODS: Thirty Goto-Kakizaki (GK) rats were randomly divided into three groups: RYGB operation, sham operation, and food restriction groups. Ten Wistar rats were used as non-diabetic control. The body weight and food consumption of rats were recorded 1 week before or every week after surgery. The fasting blood sugar and oral glucose tolerance test were performed using blood glucose meter. The levels of plasma insulin or glucagon-like peptide-1 (GLP-1) were evaluated by enzyme-linked immunosorbent assay. The insulin resistance was quantified using homeostasis model assessment method. The expression of GLP-1 receptor, Bcl-2, Bax, and caspase-3 was determined by Western blotting. RESULTS: Our results revealed that RYGB efficiently improved both glucose tolerance and insulin resistance in GK diabetic rats by upregulating GLP-1/GLP-1R expression. In addition, GLP-1R agonist exendin-4 dose-dependently increased insulin secretion in RIN-m5F cells and regulated the proliferation and apoptosis of these cells. CONCLUSIONS: RYGB provides a valuable therapeutic option for patients with type 2 diabetes. GLP-1 may contribute to the regulation of pancreatic β-cell function through its receptor following RYGB.[Abstract] [Full Text] [Related] [New Search]