The Role of β-Cell Function and Insulin Sensitivity in the Remission of Type 2 Diabetes after Gastric Bypass Surgery

Abstract

In morbid obesity, Roux-en-Y gastric bypass causes rapid and profound metabolic adaptations; insulin sensitivity improves in proportion to the weight loss, and β-cell glucose sensitivity increases independently of weight loss. Over a period of 1 yr after surgery, diabetes remission depends on the starting degree of β-cell dysfunction.

Prediction of Diabetes Remission in Morbidly Obese Patients After Roux-en-Y Gastric Bypass

“…It is assumed that the elevated C-peptide levels in morbidly obese diabetic patients implicate well-preserved pancreatic β cell function capable enough to compensate for the increased insulin resistance. Nannipieri et al suggested that on a background of better β cell function, improvement in β cell glucose sensitivity after RYGB represents the major determinant in type 2 diabetes remission [30]. In the similar sense, younger age and no insulin requirement, which are known to indirectly reflect better β cell function, also served as predictors of diabetes remission in the present study, although the significance varied across the different types of analyses.…”

Surgical Management of Obesity and the Relationship to Cardiovascular Disease

“…During the 12 months after RYGB, the likelihood and extent of diabetes remission is dependent on the degree of preoperative β-cell dysfunction. 91 In large clinical studies, the eventual degree of weight loss generally correlated with the extent of metabolic benefit derived from surgery. EWL paralleled the magnitude of biochemical responses in studies by Schauer et al 92 …”

Remission of type 2 diabetes after omega loop gastric bypass for morbid obesity

“…It is clear that the risk of developing T2D increases with an increase in BMI, but the severity of T2D in patients with a low BMI seems to implicate a deficiency in insulin secretion rather than a phenomenon of insulin resistance [22,25,27,35]. The duration of diabetes would confirm this hypothesis, with a better (reserve) for insulin secretion in obese patients recently affected by T2D [3,10,[21][22][23][24][25][26][27]30].…”