title: Weight loss and incretin responsiveness improve glucose control independently after gastric bypass surgery.
abstract: BACKGROUND
  The aim of the present study was to determine the mechanisms underlying Type 2 diabetes remission after gastric bypass (GBP) surgery by characterizing the short- and long-term changes in hormonal determinants of blood glucose.
  
  
  METHODS
  Eleven morbidly obese women with diabetes were studied before and 1, 6, and 12 months after GBP; eight non-diabetic morbidly obese women were used as controls. The incretin effect was measured as the difference in insulin levels in response to oral glucose and to an isoglycemic intravenous challenge. Outcome measures were glucose, insulin, C-peptide, proinsulin, amylin, glucagon, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) levels and the incretin effect on insulin secretion.
  
  
  RESULTS
  The decrease in fasting glucose (r = 0.724) and insulin (r = 0.576) was associated with weight loss up to 12 months after GBP. In contrast, the blunted incretin effect (calculated at 22%) that improved at 1 month remained unchanged with further weight loss at 6 (52%) and 12 (52%) months. The blunted incretin (GLP-1 and GIP) levels, early phase insulin secretion, and other parameters of β-cell function (amylin, proinsulin/insulin) followed the same pattern, with rapid improvement at 1 month that remained unchanged at 1 year.
  
  
  CONCLUSIONS
  The data suggest that weight loss and incretins may contribute independently to improved glucose levels in the first year after GBP surgery.
authors.affiliation: New York Obesity Research Center, St Luke’s/Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York, USA.
authors.forename: Mousumi
authors.initials: M
authors.lastname: Bose
authors.forename: Julio
authors.initials: J
authors.lastname: Teixeira
authors.forename: Blanca
authors.initials: B
authors.lastname: Olivan
authors.forename: Baani
authors.initials: B
authors.lastname: Bawa
authors.forename: Sara
authors.initials: S
authors.lastname: Arias
authors.forename: Sriram
authors.initials: S
authors.lastname: Machineni
authors.forename: F Xavier
authors.initials: FX
authors.lastname: Pi-Sunyer
authors.forename: Philipp E
authors.initials: PE
authors.lastname: Scherer
authors.forename: Blandine
authors.initials: B
authors.lastname: Laferrère
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D005215:Fasting; D005260:Female; D015390:Gastric Bypass; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D005951:Glucose Tolerance Test; D006801:Humans; D054795:Incretins / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D020738:Leptin / Q000097:blood; D008875:Middle Aged; D009767:Obesity, Morbid / Q000150:complications / Q000601:surgery*; D011184:Postoperative Period; D013270:Stomach / Q000601:surgery*; D015431:Weight Loss / Q000502:physiology*
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D054795:Incretins; D007328:Insulin; D020738:Leptin; D052216:Glucagon-Like Peptide 1; D005934:Glucagon