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.
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.
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.
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: email@example.com.