389-P: Comparison of Hormonal Response to a Mixed-Meal Challenge in Individuals with Hypoglycemia after Sleeve Gastrectomy vs. Gastric Bypass

Abstract

Objective: Exaggerated post-prandial incretin and insulin responses are well-documented in post-bariatric surgery hypoglycemia (PBH) after Roux-en-Y gastric bypass (RYGB). However, less is known about PBH after sleeve gastrectomy (SG). Thus, we sought to compare meal-stimulated hormonal response in those with PBH after SG vs. RYGB. Methods: We enrolled 20 RYGB (7 with and 13 without PBH) and 23 SG (12 with and 11 without PBH) who underwent bariatric surgery at our institution. PBH was defined as a postprandial interstitial or plasma glucose <55 mg/dl on continuous glucose monitor (5-days as outpatient, Dexcom) or 4-hour mixed meal tolerance test (MTT). Plasma samples from MTT were used to measure glucose, insulin, glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP). We used Kruskal Wallis Test to compare the difference in glucose or hormones across 4 groups (with and without PBH after SG or RYGB). Results: Participants (N=43) were on average 5 years since surgery, with mean age of 50 years, mean preoperative BMI of 48 kg/m2, 81% female, 61% Caucasian, 53% post SG. There were no differences in fasting glucose (p=0.38) or fasting insulin (p=0.34) across the 4 groups. Among those with PBH, the SG group showed a lower peak glucose (131.8 mg/dl, p<0.01), similar nadir glucose (59.6 mg/dl, p=0.18), peak insulin (68.7 mU/L, p<0.01) and peak GLP-1 (15.3 pM, p<0.01) and differed in overall hormonal response (AUC 0-240min) with lower insulin (3956.1 mU/L/min, p<0.01), lower GLP-1 (2498.9 pM/min, p<0.01) and higher GIP (51335.4 pM/min, p=0.05) compared to RYGB with PBH group. Conclusion: Among those with PBH, the SG group showed less glycemic excursion and different hormonal profiles including lower insulin, GLP-1 and higher GIP responses to MTT compared to the RYGB group. Future studies are needed to better understand the differential contribution of insulin and non-insulin mediated mechanisms behind PBH after SG vs. RYGB. Disclosure C. Lee: Consultant; Self; XOMA Corporation. Research Support; Self; Eiger BioPharmaceuticals. T. Brown: None. M. Schweitzer: Consultant; Self; Ethicon, Inc. T. Magnuson: None. J. Clark: None. Funding National Institutes of Health