2075-P: Insulin Resistance Improved at Six Months following Bariatric Surgery Despite Accelerated Lipolysis and Accumulation of Lipid-Derived Acylcarnitines

Abstract

Background: Accelerated lipolysis and the accumulation of incomplete products of fatty acid metabolism may contribute to insulin resistance (IR). It remains unclear whether the improvement in IR during the early period following bariatric surgery could be related to changes in lipid metabolism. Aims and Hypothesis: In this study, we compared the rates of lipolysis, lipid-related acylcarnitines (ACs) and IR in morbidly obese individuals at baseline, 6-months after bariatric surgery and with lean controls. Methods: 10 morbidly obese individuals scheduled for sleeve gastrectomy and 14 lean controls were recruited. IR was quantified using OGTT while body composition was measured using the 2H2O technique or DXA scans. Glycerol flux represents whole-body lipolysis and was measured using 2H5-glycerol infusion. Plasma lipid-derived ACs were measured using mass spectrometry as an indicator of complete fatty acid oxidation. Obese subjects were reassessed 6-months after bariatric surgery. Results: Compared to lean controls, obese subjects had significantly higher fat mass (50.7 ± 1.9 vs. 16.8 ± 1.0 kg) and were significantly more IR. They had higher HOMA-IR (6.6 ± 1.0 vs. 1.43 ± 0.31), glucose and insulin AUC after OGTT. Glycerol flux (16098.1 ± 1136.2 vs. 7266.20± 497.66 umol/h), plasma glycerol (117.13 ± 10.96 vs, 46.79± 3.15 umol/L), C14 (0.225 ± 0.079 vs. 0.042± 0.012) and C16 (0.136 ± 0.016 vs. 096 ± 0.003 umol/L) ACs were significantly higher in the obese individuals. 8 subjects returned at 6-months and lost 19% of their total weight, 29% of fat mass and had a 68% decrease in HOMA-IR. Glycerol flux, plasma glycerol, C14 and C18 ACs however did not show any difference compared to baseline and remained significantly higher compared to the lean controls. Conclusion: IR improved 6-months following sleeve gastrecotmy despite accelerated lipolysis and accumulation of byproducts of incomplete fatty acid metabolism. Disclosure H. Tan: None. J.W. Hsu: None. J. Kovalik: None. C. Khoo: None. S. Chacko: None. S. Ganguly: None. E. Tai: Advisory Panel; Self; Amgen Inc., BASF. O. Lai: None. E. Lim: None. F. Jahoor: None.