Objective: Biliopancreatic diversion (BPD) resolves type 2 diabetes in near totality of morbidly obeses [BMI (body mass index) ≥35 kg/m2]. However, studies of BPD effect in BMI range 25.0 to 34.9 kg/m2, including about 90% of diabetic patients, are lacking.
Materials and Methods: If BPD effects are independent of weight changes, they should be maintained in patients who, being mildly obese or overweight, will lose little or no weight after operation. Thirty type 2 diabetic patients with BMI 25 to 34.9 were submitted to BPD and monitored 12 months. Thirty-eight diabetic patients selected from a large database, kept 1 year on medical therapy, served as controls.
Results: Nineteen male and 11 female. Mean age 56.4 ± 7.4 years, weight 84.8 ± 11.1 kg, BMI 30.6 ± 2.9 kg/m2, waist circumference 104 ± 9.4 cm, diabetes duration 11.2 ± 6.9 years, HbA1c 9.3±1.5. Twelve patients on insulin. Fifteen (2 F) with BMI < 30 (mean: 28.1). No mortality or major adverse events occurred. BMI progressively decreased, stabilizing around 25 since the fourth month, without excessive weight loss. One year after BPD, mean HbA1c was 6.3%±0.8, with 25 patients (83%) controlled (HbA1c≤7%) on free diet, without antidiabetics, and the remaining improved. Acute insulin response to intravenous glucose had increased from 1.2 ± 2.9 to 4.2 ± 4.4 μIU/mL. Diabetes resolution correlated positively with BMI. HbA1c decreased at 1 year in the control group, along with an overall increased amount of antidiabetic therapy.
Conclusions: BPD improves or resolves diabetes in BMI 25 to 35 without causing excessive weight loss, its action being on insulin sensitivity and beta-cell function. The strikingly different response between morbidly obese and low BMI patients might depend on different beta-cell defect. ClinicalTrials.gov Identifier: NCT00996294
The effects of BPD on T2DM in 30 type 2 diabetic patients with BMI 25–35 was studied. A striking improvement of glycemic control was observed in all cases with BMI 30–35, and in most with BMI 25–30. A close correlation was found between BMI and metabolic outcome, which might depend on different beta-cell defects.
*Department of Surgery.
††Department of Endocrinology University of Genoa, Italy.
‡‡Department of Surgery, School of Medicine, Charles University, Prague, Czech Republic.
Reprints: Nicola Scopinaro, DISC – Università di Genova, Azienda Ospedaliera Universitaria “San Martino”, Largo Rosanna Benzi, 8, 16132 Genova, Italy. E-mail: firstname.lastname@example.org.