Increased binding of insulin to mononuclear blood cells following gastric bypass for morbid obesity

The insulin resistance of obesity may be related to “down-regulation” of insulin receptor number and/or affinity in vivo which is reflected quantitatively by decreased insulin binding to blood mononuclear cells in vitro. To determine the effect of surgically induced weight loss on insulin receptor function, blood mononuclear cell insulin binding was measured in normal, morbidly obese (mean 270.0 ± 21.3% of ideal body weight), and post-gastric bypass patients (mean 45.3 ± 13.5 kg weight loss) who, 2 years postoperatively, were still 136 ± 27% of ideal weight. In vitro, at all physiologic concentrations of insulin the morbidly obese group bound significantly less insulin than either the postoperative patients or normal controls. There was a two- to three-fold reduction in receptor number, with no substantial alteration of insulin binding affinity. The data suggest that surgically induced weight loss can result in “up-regulation” of insulin receptor function, and that normalization of weight is not necessary for correction of insulin receptor function in morbidly obese patients.