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.
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.
authors.affiliation: Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Liu
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhou
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.forename: Donghua
authors.initials: D
authors.lastname: Geng
authors.forename: Jingang
authors.initials: J
authors.lastname: Liu
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D015153:Blotting, Western; D001835:Body Weight; D002460:Cell Line; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism / Q000601:surgery*; D004435:Eating; D004797:Enzyme-Linked Immunosorbent Assay; D000077270:Exenatide; D015390:Gastric Bypass; D052216:Glucagon-Like Peptide 1 / Q000097:blood*; D000067757:Glucagon-Like Peptide-1 Receptor; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood* / Q000378:metabolism; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010455:Peptides / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018027:Receptors, Glucagon / Q000819:agonists / Q000378:metabolism; D014688:Venoms / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; C000593835:Glp1r protein, rat; D000067757:Glucagon-Like Peptide-1 Receptor; D007328:Insulin; D010455:Peptides; D018027:Receptors, Glucagon; D014688:Venoms; D052216:Glucagon-Like Peptide 1; D000077270:Exenatide