Gastric Feeding Reduces Postprandial Glucose Excursions and GLP-1 Production in Gastric Bypass Patients

Presentation Number: MON 583
Date of Presentation: April 3rd, 2017

Dawn Belt Davis*1, Jad Khoraki2, Sirinart Sirinvaravong2, Jee Young Han2 and Guilherme M Campos2
1University of Wisconsin - Madison, Madison, WI, 2University of Wisconsin - Madison

Abstract

Roux en Y gastric bypass (RYGB) surgery imparts dramatic metabolic benefits, yet in some patients can lead to late-onset postprandial hypoglycemia. We and others have found that RYGB results in alterations in postprandial glucose, insulin and gut hormone profiles. We conducted a study of seven subjects with RYGB and inserted a gastrostomy feeding tube into their bypassed stomach. We then performed mixed meal tolerance tests to compare oral feeding to feeding through the bypassed stomach. All subjects then underwent gastric bypass reversal and mixed meal tolerance test was repeated. We previously published dramatic improvement in hypoglycemic symptoms after reversal and recently reported reduction in postprandial glucose, insulin, and GLP-1 after reversal and with gastrostomy tube feeding in these subjects. These data support a conclusion that the route of food delivery and the timing of absorption are critical in determining postprandial glycemic response, and that pancreatic function is not altered in gastric-bypass hypoglycemic patients. Here, we further analyze data to compare those subjects with reversal to normal anatomy (n=3) vs. sleeve gastrectomy (n=4). Postprandial hypoglycemia has not been widely reported in sleeve gastrectomy patients, despite similar improvement in metabolic parameters as RYGB. We found that postprandial glucose, insulin, GLP-1, and PYY excursions were not significantly different between these groups (p=0.79-0.96), and all reversal patients had dramatically lower excursions when compared to their own pre-reversal RYGB feeding. Additionally, weight gain after reversal of RYGB was not different over an average of 20 months of follow up (44.5 lbs gain sleeve vs. 28.5 lbs gain normal, p=0.57). This suggests that reversal of RYGB to sleeve gastrectomy restores normal postprandial glucose and hormonal responses. One of our seven subjects had no history of symptomatic hypoglycemia, yet still had very similar elevations in postprandial glucose, insulin, and GLP-1 compared to symptomatic subjects. It appears that postprandial responses are an inherent feature of the route of food delivery, and do not seem highly specific for those suffering from gastric bypass-related hypoglycemia. Hypoglycemia after gastric bypass surgery remains a poorly understood phenomenon with limited published information on effective therapy. Our study uniquely followed these patients prospectively with mixed meal tolerance testing at baseline, with a gastrostomy tube into the excluded stomach, and after gastric bypass reversal. We are able to conclude that gastric feeding through bypassed stomach, sleeve gastrectomy, or restoration of normal stomach results reduced postprandial glucose and GLP-1 excursions and is a viable treatment strategy for RYGB hypoglycemia.

 

Nothing to Disclose: DBD, JK, SS, JYH, GMC