Guilherme M Campos1, Charlotte Rabl2, Peter J Havel3, Madhu Rao4, Jean-Marc Schwarz5, Morris Schambelan4, Kathleen Mulligan4. 1. Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; Department of Surgery, University of California San Francisco, San Francisco, California. Electronic address: campos@surgery.wisc.edu. 2. Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin; Department of Surgery, University of California San Francisco, San Francisco, California; Department of Surgery, Paracelsus Medical University, Salzburg, Austria. 3. Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California Davis, Davis, California. 4. Department of Medicine, University of California San Francisco, San Francisco, California. 5. Touro University-California, Vallejo, California.
Abstract
BACKGROUND: Changes in the multiple mechanisms that regulate glucose metabolism after gastric bypass (RYGB) are still being unveiled. The objective of this study was to compare the changes of glucose and pancreatic hormones [C-peptide, glucagon, and pancreatic polypeptide (PP)] during a meal tolerance test (MTT) and steady-state insulin and free fatty acid (FFA) concentrations during euglycemic-hyperinsulinemic clamp 14 days and 6 months after RYGB in morbidly obese nondiabetic patients. METHODS: Two groups were studied at baseline and at 14 days: the RYGB followed by caloric restriction group (RYGB, n = 12) and the equivalent caloric restriction alone group (Diet, n = 10), to control for energy intake and weight loss. The RYGB group was studied again at 6 months to assess the changes after substantial weight loss. During MTT, the early and overall changes in glucose and pancreatic hormone concentrations were determined, and during the clamp, steady-state insulin and FFA concentrations were assessed. RESULTS: After 14 days, RYGB patients had enhanced postprandial glucose, C-peptide, and glucagon responses, and decreased postprandial PP concentrations. Steady-state insulin concentrations were decreased at 14 days only in RYGB patients, and FFA increased in both groups. Six months after RYGB and substantial weight loss, the decrease in insulin concentrations during clamp persisted, and there were further changes in postprandial glucose and glucagon responses. FFA concentrations during clamp were significantly lower at 6 months, relative to presurgical values. CONCLUSIONS: In morbidly obese nondiabetic patients, RYGB produces early changes in postmeal glucose, C-peptide, glucagon, and PP responses, and it appears to enhance insulin clearance early after RYGB and improve insulin sensitivity in adipose tissue at 6 months postsurgery. The early changes cannot be explained by caloric restriction alone.
BACKGROUND: Changes in the multiple mechanisms that regulate glucose metabolism after gastric bypass (RYGB) are still being unveiled. The objective of this study was to compare the changes of glucose and pancreatic hormones [C-peptide, glucagon, and pancreatic polypeptide (PP)] during a meal tolerance test (MTT) and steady-state insulin and free fatty acid (FFA) concentrations during euglycemic-hyperinsulinemic clamp 14 days and 6 months after RYGB in morbidly obese nondiabeticpatients. METHODS: Two groups were studied at baseline and at 14 days: the RYGB followed by caloric restriction group (RYGB, n = 12) and the equivalent caloric restriction alone group (Diet, n = 10), to control for energy intake and weight loss. The RYGB group was studied again at 6 months to assess the changes after substantial weight loss. During MTT, the early and overall changes in glucose and pancreatic hormone concentrations were determined, and during the clamp, steady-state insulin and FFA concentrations were assessed. RESULTS: After 14 days, RYGB patients had enhanced postprandial glucose, C-peptide, and glucagon responses, and decreased postprandial PP concentrations. Steady-state insulin concentrations were decreased at 14 days only in RYGB patients, and FFA increased in both groups. Six months after RYGB and substantial weight loss, the decrease in insulin concentrations during clamp persisted, and there were further changes in postprandial glucose and glucagon responses. FFA concentrations during clamp were significantly lower at 6 months, relative to presurgical values. CONCLUSIONS: In morbidly obese nondiabeticpatients, RYGB produces early changes in postmeal glucose, C-peptide, glucagon, and PP responses, and it appears to enhance insulin clearance early after RYGB and improve insulin sensitivity in adipose tissue at 6 months postsurgery. The early changes cannot be explained by caloric restriction alone.
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