title: Mechanisms of recovery from type 2 diabetes after malabsorptive bariatric surgery.
abstract: Currently, there are no data in the literature regarding the pathophysiological mechanisms involved in the rapid resolution of type 2 diabetes after bariatric surgery, which was reported as an additional benefit of the surgical treatment for morbid obesity. With this question in mind, insulin sensitivity, using euglycemic-hyperinsulinemic clamp, and insulin secretion, by the C-peptide deconvolution method after an oral glucose load, together with the circulating levels of intestinal incretins and adipocytokines, have been studied in 10 diabetic morbidly obese subjects before and shortly after biliopancreatic diversion (BPD) to avoid the weight loss interference. Diabetes disappeared 1 week after BPD, while insulin sensitivity (32.96 +/- 4.3 to 65.73 +/- 3.22 mumol . kg fat-free mass(-1) . min(-1) at 1 week and to 64.73 +/- 3.42 mumol . kg fat-free mass(-1) . min(-1) at 4 weeks; P < 0.0001) was fully normalized. Fasting insulin secretion rate (148.16 +/- 20.07 to 70.0.2 +/- 8.14 and 83.24 +/- 8.28 pmol/min per m(2); P < 0.01) and total insulin output (43.76 +/- 4.07 to 25.48 +/- 1.69 and 30.50 +/- 4.71 nmol/m(2); P < 0.05) dramatically decreased, while a significant improvement in beta-cell glucose sensitivity was observed. Both fasting and glucose-stimulated gastrointestinal polypeptide (13.40 +/- 1.99 to 6.58 +/- 1.72 pmol/l at 1 week and 5.83 +/- 0.80 pmol/l at 4 weeks) significantly (P < 0.001) decreased, while glucagon-like peptide 1 significantly increased (1.75 +/- 0.16 to 3.42 +/- 0.41 pmol/l at 1 week and 3.62 +/- 0.21 pmol/l at 4 weeks; P < 0.001). BPD determines a prompt reversibility of type 2 diabetes by normalizing peripheral insulin sensitivity and enhancing beta-cell sensitivity to glucose, these changes occurring very early after the operation. This operation may affect the enteroinsular axis function by diverting nutrients away from the proximal gastrointestinal tract and by delivering incompletely digested nutrients to the ileum.
authors.affiliation: Dipartimento di Medicina Interna, Catholic University, Largo A. Gemelli, 8, 00168 Rome, Italy. gmingrone@rm.unicatt.it
authors.forename: Caterina
authors.initials: C
authors.lastname: Guidone
authors.forename: Melania
authors.initials: M
authors.lastname: Manco
authors.forename: Elena
authors.initials: E
authors.lastname: Valera-Mora
authors.forename: Amerigo
authors.initials: A
authors.lastname: Iaconelli
authors.forename: Donatella
authors.initials: D
authors.lastname: Gniuli
authors.forename: Andrea
authors.initials: A
authors.lastname: Mari
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Nanni
authors.forename: Marco
authors.initials: M
authors.lastname: Castagneto
authors.forename: Menotti
authors.initials: M
authors.lastname: Calvani
authors.forename: Geltrude
authors.initials: G
authors.lastname: Mingrone
mesh_terms: D052242:Adiponectin / Q000097:blood; D019540:Area Under Curve; D050110:Bariatric Surgery; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D015309:Glucose Clamp Technique; D006801:Humans; D007328:Insulin / Q000097:blood; D008875:Middle Aged; D009767:Obesity, Morbid / Q000150:complications / Q000503:physiopathology / Q000601:surgery*; D011184:Postoperative Period; D015431:Weight Loss
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin