Authors: S Salinari A Bertuzzi A Iaconelli M Manco G Mingrone
Publish Date: 2008/05/06
Volume: 51, Issue: 7, Pages: 1276-
Abstract
We have previously demonstrated that type 2 diabetes resolves after bariatric surgery To study the role of NEFA in the prompt normalisation of beta cell glucose sensitivity insulin secretion and beta cell glucose and lipid metabolism were investigated by a model of nutrientstimulated insulin secretion using a multiplemeal testHourly glucose Cpeptide and NEFA were measured in nine morbidly obese type 2 diabetic patients before and 1 week after bariatric surgery and in six matched healthy volunteers over 24 h A mathematical model of glucose–NEFA comodulation of insulin secretion rate ISR was used to compute ISR and βoxidation Insulin sensitivity was measured by an OGTT minimal modelBeta cell sensitivity to glucose and NEFA was doubled after surgery while the 24 h insulin secretion decreased from 2771 ± 1444 to 1980 ± 1076 nmol/m2 p 002 Insulin sensitivity was restored The βoxidation rate of beta cells was completely normalised from 0032 ± 0012 × 10−12 to 0103 ± 0031 × 10−12 mmol/min per cell p 0005 The best predictor of beta cell function improvement was the duration of diabetesBariatric surgery in type 2 diabetes restores βoxidation in beta cells doubles glucose–NEFA sensitivity and reverses diabetes It is likely that ISR is reduced to match insulinsensitivity normalisation in spite of no significant reduction in NEFA levels We hypothesise that insulin sensitivity normalisation might appear as a consequence of nutrient exclusion from proximal intestinal transit and that secondarily the need for insulin secretion diminishes The insulin sensitivity increase is much higher than usually obtained by insulinsensitising agents and is independent of weight changes
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