Meera Shah1, Marcello C Laurenti2, Chiara Dalla Man3, Jing Ma4, Claudio Cobelli5, Robert A Rizza6, Adrian Vella7. 1. Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: shah.meera@mayo.edu. 2. Department of Information Engineering, University of Padua, Via Gradenigo 6A, Padua 35131, Italy. Electronic address: laurenti.marcello@mayo.edu. 3. Department of Information Engineering, University of Padua, Via Gradenigo 6A, Padua 35131, Italy. Electronic address: chiara.dallaman@dei.unipd.it. 4. Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: ma.jing@mayo.edu. 5. Department of Information Engineering, University of Padua, Via Gradenigo 6A, Padua 35131, Italy. Electronic address: cobelli@dei.unipd.it. 6. Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: rizza.robert@mayo.edu. 7. Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. Electronic address: vella.adrian@mayo.edu.
Abstract
Glucagon-Like Peptide-1 (GLP-1) is an insulin secretagogue which is elevated after Roux-en-Y Gastric Bypass (RYGB). However, its contribution to glucose metabolism after RYGB remains uncertain. AIMS: We tested the hypothesis that GLP-1 lowers postprandial glucose concentrations and improves β-cell function after RYGB. MATERIALS AND METHODS: To address these questions we used a labeled mixed meal to assess glucose metabolism and islet function in 12 obese subjects with type 2 diabetes studied before and four weeks after RYGB. During the post-RYGB study subjects were randomly assigned to receive an infusion of either saline or Exendin-9,39 a competitive antagonist of GLP-1 at its receptor. Exendin-9,39 was infused at 300 pmol/kg/min for 6 h. All subjects underwent RYGB for medically-complicated obesity. RESULTS: Exendin-9,39 resulted in increased integrated incremental postprandial glucose concentrations (181 ± 154 vs. 582 ± 129 mmol per 6 h, p = 0.02). In contrast, this was unchanged in the presence of saline (275 ± 88 vs. 315 ± 66 mmol per 6 h, p = 0.56) after RYGB. Exendin-9,39 also impaired β-cell responsivity to glucose but did not alter Disposition Index (DI). CONCLUSIONS: These data indicate that the elevated GLP-1 concentrations that occur early after RYGB improve postprandial glucose tolerance by enhancing postprandial insulin secretion.
RCT Entities:
Glucagon-Like Peptide-1 (GLP-1) is an insulin secretagogue which is elevated after Roux-en-Y Gastric Bypass (RYGB). However, its contribution to glucose metabolism after RYGB remains uncertain. AIMS: We tested the hypothesis that GLP-1 lowers postprandial glucose concentrations and improves β-cell function after RYGB. MATERIALS AND METHODS: To address these questions we used a labeled mixed meal to assess glucose metabolism and islet function in 12 obese subjects with type 2 diabetes studied before and four weeks after RYGB. During the post-RYGB study subjects were randomly assigned to receive an infusion of either saline or Exendin-9,39 a competitive antagonist of GLP-1 at its receptor. Exendin-9,39 was infused at 300 pmol/kg/min for 6 h. All subjects underwent RYGB for medically-complicated obesity. RESULTS:Exendin-9,39 resulted in increased integrated incremental postprandial glucose concentrations (181 ± 154 vs. 582 ± 129 mmol per 6 h, p = 0.02). In contrast, this was unchanged in the presence of saline (275 ± 88 vs. 315 ± 66 mmol per 6 h, p = 0.56) after RYGB. Exendin-9,39 also impaired β-cell responsivity to glucose but did not alter Disposition Index (DI). CONCLUSIONS: These data indicate that the elevated GLP-1 concentrations that occur early after RYGB improve postprandial glucose tolerance by enhancing postprandial insulin secretion.
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