Abstract

Although literature describes the influence of bariatric surgery on insulin sensitivity (IS) showing improvement in metabolic parameters, including sustained remission of type 2 diabetes and reduction in cardiovascular disease, the underlying mechanisms remain unclear. Changes in SAT following bariatric surgery make it a key site for investigating mechanisms of glucose control. To test whether changes in SAT are related to improved IS following bariatric surgery, we quantified adipose cell size distribution in SAT harvests, in addition to quantifying insulin resistance (IR) using the steady-state plasma glucose (SSPG) test in 57 obese subjects undergoing bariatric surgery at baseline and one year post surgery. We compared IR and SAT size variables in the post-surgical subjects to those of BMI-matched non-surgical controls. Surgery subjects (n=57) were healthy, morbidly obese men and women without diabetes, ages 23-70, with BMI > 35 kg/m^2, who underwent bariatric surgery, while controls (n=43) were healthy, men and women without diabetes ages 23-70 years with BMIs 22-38.3kg/m^2. Of the surgery subjects, 14 were available at 1 year post-surgery for comparison with controls. Compared to pre-surgery, post-surgery results demonstrated a decrease in average BMI, weight, SSPG, peak diameter, nadir, and percent small cells (p<.05). Compared to the controls (BMI 30.9 +- 4.0 kg/m^2), the post-surgical subjects (BMI 30.5 +/- 3.8 kg/m^2) demonstrated reduced IR, percent small cells, and adipose cell peak diameters, p<0.001. After surgery, SAT exhibits features of healthier fat cells compared to controls, which may account for their lower IR. Independent of weight loss, adipocyte cell qualities may play a role in the improvement in IS due to bariatric surgery. These observations have implications in treatments targeting type 2 diabetes and cardiovascular disease because manipulating fat cell size and percent of small cells may provide a path to improving IS. Disclosure A. Lenz: None. T. Mclaughlin: Board Member; Self; January, Inc. E. J. Zanley: None. Funding American Heart Association; National Institutes of Health

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