title: Acute effects of gastric bypass versus gastric restrictive surgery on beta-cell function and insulinotropic hormones in severely obese patients with type 2 diabetes.
abstract: BACKGROUND
  Hyperglycemia resolves quickly after bariatric surgery, but the underlying mechanism and the most effective type of surgery remains unclear.
  
  
  OBJECTIVE
  To examine glucose metabolism and beta-cell function in patients with type 2 diabetes mellitus (T2DM) after two types of bariatric intervention; Roux-en-Y gastric bypass (RYGB) and gastric restrictive (GR) surgery.
  
  
  METHODS
  Prospective, nonrandomized, repeated-measures, 4-week, longitudinal clinical trial.
  
  
  METHODS
  In all, 16 T2DM patients (9 males and 7 females, 52+/-14 years, 47+/-9 kg m(-2), HbA1c 7.2+/-1.1%) undergoing either RYGB (N=9) or GR (N=7) surgery.
  
  
  METHODS
  Glucose, insulin secretion, insulin sensitivity at baseline, and 1 and 4 weeks post-surgery, using hyperglycemic clamps and C-peptide modeling kinetics; glucose, insulin secretion and gut-peptide responses to mixed meal tolerance test (MMTT) at baseline and 4 weeks post-surgery.
  
  
  RESULTS
  At 1 week post-surgery, both groups experienced a similar weight loss and reduction in fasting glucose (P<0.01). However, insulin sensitivity increased only after RYGB, (P<0.05). At 4 weeks post-surgery, weight loss remained similar for both groups, but fasting glucose was normalized only after RYGB (95+/-3 mg 100 ml(-1)). Insulin sensitivity improved after RYGB (P<0.01) and did not change with GR, whereas the disposition index remained unchanged after RYGB and increased 30% after GR (P=0.10). The MMTT elicited a robust increase in insulin secretion, glucagon-like peptide-1 (GLP-1) levels and beta-cell sensitivity to glucose only after RYGB (P<0.05).
  
  
  CONCLUSIONS
  RYGB provides a more rapid improvement in glucose regulation compared with GR. This improvement is accompanied by enhanced insulin sensitivity and beta-cell responsiveness to glucose, in part because of an incretin effect.
authors.affiliation: Endocrinology and Metabolism Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. kashyas@ccf.org
authors.forename: S R
authors.initials: SR
authors.lastname: Kashyap
authors.forename: S
authors.initials: S
authors.lastname: Daud
authors.forename: K R
authors.initials: KR
authors.lastname: Kelly
authors.forename: A
authors.initials: A
authors.lastname: Gastaldelli
authors.forename: H
authors.initials: H
authors.lastname: Win
authors.forename: S
authors.initials: S
authors.lastname: Brethauer
authors.forename: J P
authors.initials: JP
authors.lastname: Kirwan
authors.forename: P R
authors.initials: PR
authors.lastname: Schauer
mesh_terms: D050110:Bariatric Surgery / Q000379:methods*; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D001835:Body Weight; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000601:surgery; D005260:Female; D015390:Gastric Bypass / Q000379:methods; D005768:Gastrointestinal Hormones / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000378:metabolism / Q000601:surgery*; D011446:Prospective Studies; D015431:Weight Loss
chemical_list: D001786:Blood Glucose; D005768:Gastrointestinal Hormones; D007328:Insulin; D052216:Glucagon-Like Peptide 1