title: Restoration of acute insulin response in T2DM subjects 1 month after biliopancreatic diversion.
abstract: OBJECTIVE
  Biliopancreatic diversion (BPD) restores normal glucose tolerance in a few weeks in morbid obese subjects with type 2 diabetes, improving insulin sensitivity. However, there is less known about the effects of BPD on insulin secretion. We tested the early effects of BPD on insulin secretion in obese subjects with and without type 2 diabetes.
  
  
  METHODS
  Twenty-one consecutive morbid obese subjects, 9 with type 2 diabetes (T2DM) and 12 with normal fasting glucose (NFG) were evaluated, just before and 1 month after BPD, by measuring body weight (BW), glucose, adipocitokines, homeostasis model assessment of insulin resistance (HOMA-IR), acute insulin response (AIR) to e.v. glucose and the insulinogenic index adjusted for insulin resistance ([DeltaI5/DeltaG5]/HOMA-IR).
  
  
  RESULTS
  Preoperatively, those with T2DM differed from those with NFG in showing higher levels of fasting glucose, reduced AIR (57.9 +/- 29.5 vs. 644.9 +/- 143.1 pmol/l, P < 0.01) and reduced adjusted insulinogenic index (1.0 +/- 0.5 vs. 17.6 +/- 3.9 1/mmol(2), P < 0.001). One month following BPD, in both groups BW was reduced (by approximately 11%), but all subjects were still severely obese; HOMA-IR and leptin decreased significanlty, while high-molecular weight (HMW) adiponectin and adjusted insulinogenic index increased. In the T2DM group, fasting glucose returned to non-diabetic values. AIR did not change in the NFG group, while in the T2DM group it showed a significant increase (from 58.0 +/- 29.5 to 273.8 +/- 47.2 pmol/l, P < 0.01). In the T2DM group, the AIR percentage variation from baseline was significantly related to changes in fasting glucose (r = 0.70, P = 0.02), suggesting an important relationship exists between impaired AIR and hyperglycaemia.
  
  
  CONCLUSIONS
  BPD is able to restore AIR in T2DM even just 1 month after surgery. AIR restoration is associated with normalization of fasting glucose concentrations.
authors.affiliation: Department of Endocrinology and Medicine, University of Genova, Genova, Italy.
authors.forename: Lucia
authors.initials: L
authors.lastname: Briatore
authors.forename: Barbara
authors.initials: B
authors.lastname: Salani
authors.forename: Gabriella
authors.initials: G
authors.lastname: Andraghetti
authors.forename: Cristina
authors.initials: C
authors.lastname: Danovaro
authors.forename: Elsa
authors.initials: E
authors.lastname: Sferrazzo
authors.forename: Nicola
authors.initials: N
authors.lastname: Scopinaro
authors.forename: Gian F
authors.initials: GF
authors.lastname: Adami
authors.forename: Davide
authors.initials: D
authors.lastname: Maggi
authors.forename: Renzo
authors.initials: R
authors.lastname: Cordera
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D015904:Biliopancreatic Diversion; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology; D005215:Fasting / Q000097:blood; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D000078790:Insulin Secretion; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D015431:Weight Loss / Q000502:physiology
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin