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      Removal of Duodenum Elicits GLP-1 Secretion

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          Abstract

          OBJECTIVE

          To evaluate the effect of removal of the duodenum on the complex interplay between incretins, insulin, and glucagon in nondiabetic subjects.

          RESEARCH DESIGN AND METHODS

          For evaluation of hormonal secretion and insulin sensitivity, 10 overweight patients without type 2 diabetes (age 61 ± 19.3 years and BMI 27.9 ± 5.3 kg/m 2) underwent a mixed-meal test and a hyperinsulinemic-euglycemic clamp before and after pylorus-preserving pancreatoduodenectomy for ampulloma.

          RESULTS

          All patients experienced a reduction in insulin ( P = 0.002), C-peptide ( P = 0.0002), and gastric inhibitory peptide (GIP) secretion ( P = 0.0004), while both fasting and postprandial glucose levels increased ( P = 0.0001); GLP-1 and glucagon responses to the mixed meal increased significantly after surgery ( P = 0.02 and 0.031). While changes in GIP levels did not correlate with insulin, glucagon, and glucose levels, the increase in GLP-1 secretion was inversely related to the postsurgery decrease in insulin secretion ( R 2 = 0.56; P = 0.012) but not to the increased glucagon secretion, which correlated inversely with the reduction of insulin ( R 2 = 0.46; P = 0.03) and C-peptide ( R 2 = 0.37; P = 0.04). Given that the remaining pancreas presumably has preserved intraislet anatomy, insulin secretory capacity, and α- and β-cell interplay, our data suggest that the increased glucagon secretion is related to decreased systemic insulin.

          CONCLUSIONS

          Pylorus-preserving pancreatoduodenectomy was associated with a decrease in GIP and a remarkable increase in GLP-1 levels, which was not translated into increased insulin secretion. Rather, the hypoinsulinemia may have caused an increase in glucagon secretion.

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          Author and article information

          Journal
          Diabetes Care
          Diabetes Care
          diacare
          dcare
          Diabetes Care
          Diabetes Care
          American Diabetes Association
          0149-5992
          1935-5548
          June 2013
          15 May 2013
          : 36
          : 6
          : 1641-1646
          Affiliations
          1Division of Endocrinology and Metabolic Diseases, Università Cattolica del Sacro Cuore, Rome, Italy
          2Department of Surgery, Università Cattolica del Sacro Cuore, Rome, Italy
          3Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, Denmark
          Author notes
          Corresponding author: Giovanna Muscogiuri, giovanna.muscogiuri@ 123456gmail.com .

          G.M. and T.M. contributed equally to this study.

          Article
          0811
          10.2337/dc12-0811
          3661831
          23393218
          © 2013 by the American Diabetes Association.

          Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

          Page count
          Pages: 6
          Product
          Categories
          Original Research
          Pathophysiology/Complications

          Endocrinology & Diabetes

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