Hideharu Shimizu1, Shai Eldar1, Helen M Heneghan1, Philip R Schauer1, John P Kirwan2, Stacy A Brethauer3. 1. Bariatric and Metabolic Institute, Cleveland Clinic, Cleveland, Ohio. 2. Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio; Metabolic Translational Research Center, Endocrine and Metabolism Institute, Cleveland Clinic, Cleveland, Ohio. 3. Bariatric and Metabolic Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: brethas@ccf.org.
Abstract
BACKGROUND: Potential mechanisms underlying the antidiabetic effects of Roux-en-Y gastric bypass (RYGB) include altered nutrient exposure in the gut. The aim of this study was to evaluate the effects of selective gut stimulation on glucose metabolism in an obese diabetic rat model. METHODS: Sixteen male Zucker diabetic fatty rats were randomly assigned to 1 of 2 groups: RYGB with gastrostomy tube (GT) insertion into the excluded stomach or a control group with GT insertion into the stomach. An insulin tolerance test (ITT), oral glucose tolerance test (OGTT), and mixed meal tolerance test (MMTT) were performed before and 14-28 days after surgery. A glucose tolerance test via GT (GTT-GT) and MMTT via GT were performed postoperatively. RESULTS: Postoperatively, the RYGB group had significant decreases in weight and food intake. Both the ITT and OGTT tests revealed significantly improved glucose tolerance after RYGB. The GTT-GT showed a reversal of the improved glucose tolerance in the RYGB group. In response to meal stimulation, postoperatively, the RYGB group increased glucagon-like peptide 1 (GLP-1) secretion via the oral route and peptide YY secretion by both oral and GT routes. CONCLUSION: When foregut exposure to nutrients was reversed after RYGB, the improvement in glucose metabolism was abrogated. This model can be extended to identify the role of gut in glucose homeostasis in type 2 diabetes.
BACKGROUND: Potential mechanisms underlying the antidiabetic effects of Roux-en-Y gastric bypass (RYGB) include altered nutrient exposure in the gut. The aim of this study was to evaluate the effects of selective gut stimulation on glucose metabolism in an obese diabeticrat model. METHODS: Sixteen male Zucker diabetic fatty rats were randomly assigned to 1 of 2 groups: RYGB with gastrostomy tube (GT) insertion into the excluded stomach or a control group with GT insertion into the stomach. An insulin tolerance test (ITT), oral glucose tolerance test (OGTT), and mixed meal tolerance test (MMTT) were performed before and 14-28 days after surgery. A glucose tolerance test via GT (GTT-GT) and MMTT via GT were performed postoperatively. RESULTS: Postoperatively, the RYGB group had significant decreases in weight and food intake. Both the ITT and OGTT tests revealed significantly improved glucose tolerance after RYGB. The GTT-GT showed a reversal of the improved glucose tolerance in the RYGB group. In response to meal stimulation, postoperatively, the RYGB group increased glucagon-like peptide 1 (GLP-1) secretion via the oral route and peptide YY secretion by both oral and GT routes. CONCLUSION: When foregut exposure to nutrients was reversed after RYGB, the improvement in glucose metabolism was abrogated. This model can be extended to identify the role of gut in glucose homeostasis in type 2 diabetes.
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