title: The effects of duodenal-jejunal exclusion on hormonal regulation of glucose metabolism in Goto-Kakizaki rats.
abstract: BACKGROUND
  The antidiabetic effect of bariatric surgery has been interpreted as a conceivable result of surgically induced weight loss and decreased caloric intake. However, glycemic control often occurs within days, before significant weight loss has been reached. The aim of our work was to investigate the hormones that control glycemic status in diabetes mellitus after a duodenal-jejunal exclusion in an animal model of nonobese type 2 diabetes.
  
  
  METHODS
  Twelve (12- to 14-week-old) rats (Goto-Kakizaki) randomly underwent one of the following procedures: gastrojejunal bypass (group 1, n = 6) or no intervention (controls) (group 2, n = 6). Both groups were fed with the same type and amount of diet. At basal time (preoperative) and after intervention (1 week and 1 month), weight and fasting glycemia were measured. An oral glucose tolerance test (OGTT) was realized at same times. Hormone levels (insulin, glucagons-like peptide 1 [GLP-1], glucose-dependent insulinotropic peptide [GIP], glucagon, and leptin) were measured after 20 minutes of oral glucose overload. Age-matched Goto-Kakizaki rats were used as controls for all variables.
  
  
  RESULTS
  Rats in group 1 and group 2 remained with the same weight during the protocol. The OGTT showed an improvement in glycemic levels in group 1; glucose levels were better at 1 week and 1 month after the surgery in all times of OGTT (basal, 10 minutes, and 120 minutes). Basal glucose levels at time 0 in basal time, at 1 week, and at 1 month were lower in group 1 than group 2. Postoral glucose overload levels of glucagon, insulin, GLP-1, and GIP remained unchanged during the treatment in both groups. In group 1, leptin levels had a significant decrease at 1 week and 1 month after surgery (basal time (6.1 +/- 1.6 ng/mL) versus 1 week (0.9 +/- 0.9 ng/mL) versus 1 month (0.7 +/- 0.6 ng/mL) (P < .05).
  
  
  CONCLUSIONS
  Gastrojejunal bypass in a nonobese diabetic model improves glycemic control with a significant decrease in leptin levels, without changes in enteroinsular axis (GLP-1, GIP, glucagons, and insulin levels).
authors.affiliation: Unit of Investigation, Hospital Rio Hortega, University of Valladolid, C/Los perales 16, Simancas 47310, Valladolid, Spain.
authors.forename: David
authors.initials: D
authors.lastname: Pacheco
authors.forename: Daniel Antonio
authors.initials: DA
authors.lastname: de Luis
authors.forename: Alejandro
authors.initials: A
authors.lastname: Romero
authors.forename: Manuel
authors.initials: M
authors.lastname: González Sagrado
authors.forename: Rosa
authors.initials: R
authors.lastname: Conde
authors.forename: Olatz
authors.initials: O
authors.lastname: Izaola
authors.forename: Rocío
authors.initials: R
authors.lastname: Aller
authors.forename: Alberto
authors.initials: A
authors.lastname: Delgado
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000601:surgery*; D004195:Disease Models, Animal; D015390:Gastric Bypass; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D005951:Glucose Tolerance Test; D006706:Homeostasis / Q000502:physiology*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon