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Diabetes 55:2025-2031, 2006
DOI: 10.2337/db06-0068
© 2006 by the American Diabetes Association
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Mechanisms of Recovery From Type 2 Diabetes After Malabsorptive Bariatric Surgery

Caterina Guidone1, Melania Manco1, Elena Valera-Mora1, Amerigo Iaconelli1, Donatella Gniuli1, Andrea Mari2, Giuseppe Nanni3, Marco Castagneto3, Menotti Calvani1, and Geltrude Mingrone1

Department of Internal Medicine, Catholic University, School of Medicine, Rome, Italy
2 Metabolic Modeling Unit, Institute of Biomedical Engineering, National Research Council, Padova, Italy
3 Department of Surgery, CNR Centro di Fisiopatologia dello Shock, Catholic University, School of Medicine, Rome, Italy

Address correspondence and reprint requests to Prof. Geltrude Mingrone, Dipartimento di Medicina Interna, Catholic University, Largo A. Gemelli, 8, 00168 Rome, Italy. E-mail: gmingrone{at}rm.unicatt.it

Abbreviations: AUC, area under the curve; BPD, biliopancreatic diversion; FFM, fat-free mass; GIP, gastrointestinal polypeptide; GLP-1, glucagon-like peptide 1; OGTT, oral glucose tolerance test

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 µmol · kg fat-free mass–1 · min–1 at 1 week and to 64.73 ± 3.42 µmol · 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 m2; P < 0.01) and total insulin output (43.76 ± 4.07 to 25.48 ± 1.69 and 30.50 ± 4.71 nmol/m2; P < 0.05) dramatically decreased, while a significant improvement in ß-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 ß-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.


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