Impaired early-phase suppression of glucagon secretion after glucose load is associated with insulin requirement during pregnancy in gestational diabetes.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Additional Information
    • Source:
      Publisher: Asian Association for the Study of Diabetes and Blackwell Pub. Asia Country of Publication: Japan NLM ID: 101520702 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2040-1124 (Electronic) Linking ISSN: 20401116 NLM ISO Abbreviation: J Diabetes Investig Subsets: MEDLINE
    • Publication Information:
      Original Publication: Tokyo : Asian Association for the Study of Diabetes and Blackwell Pub. Asia
    • Subject Terms:
      Diabetes Mellitus, Type 2/*drug therapy ; Diabetes, Gestational/*drug therapy ; Glucagon/*metabolism ; Glucose Intolerance/*drug therapy ; Hypoglycemic Agents/*therapeutic use ; Insulin/*therapeutic use; Adult ; Biomarkers/analysis ; Blood Glucose/analysis ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Diabetes, Gestational/metabolism ; Diabetes, Gestational/pathology ; Female ; Follow-Up Studies ; Glucose Intolerance/metabolism ; Glucose Intolerance/pathology ; Glucose Tolerance Test ; Humans ; Insulin/blood ; Pregnancy ; Prognosis ; Prospective Studies
    • Abstract:
      Aims/introduction: The role of glucagon abnormality has recently been reported in type 2 diabetes; however, its role in gestational diabetes mellitus (GDM) is still unknown. The glucose intolerance in GDM is heterogeneous, and not all patients require insulin treatment during pregnancy. Here, we investigated whether glucagon abnormality is associated with the requirement for insulin treatment during pregnancy.
      Materials and Methods: A total of 49 pregnant women diagnosed with GDM were enrolled. They underwent a 75-g oral glucose tolerance test during mid-gestation, and we measured their plasma glucagon levels (by a new sandwich enzyme-linked immunosorbent assay) at fasting (0 min), and at 30, 60 and 120 min after glucose load in addition to the levels of plasma glucose and serum insulin. All participants underwent another oral glucose tolerance test at postpartum.
      Results: Of the 49 patients, 15 required insulin treatment (Insulin group) and 34 were treated with diet therapy alone until delivery (Diet group). The early-phase glucagon secretion after glucose load, as determined by the changes in glucagon from the baseline to 30 min, was paradoxically augmented during mid-gestation in the Insulin group, but not in the Diet group. The impaired glucagon suppression during mid-gestation in the Insulin group was not associated with insulin secretory/sensitivity indexes studied, and was ameliorated postpartum, although the plasma glucose levels remained higher in the Insulin group versus the Diet group.
      Conclusions: Impaired early-phase suppression of glucagon could be associated with the requirement for insulin treatment during pregnancy in patients with GDM.
      (© 2019 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)
    • References:
      Diabetes Res Clin Pract. 2006 Jun;72(3):298-301. (PMID: 16325298)
      Diabetes Res Clin Pract. 2014 Jan;103(1):20-5. (PMID: 24405981)
      Diabetes Res Clin Pract. 2015 Mar;107(3):400-6. (PMID: 25631609)
      Diabetologia. 2014 Sep;57(9):1919-26. (PMID: 24891019)
      Am J Obstet Gynecol. 1991 Dec;165(6 Pt 1):1667-72. (PMID: 1750458)
      Endocr J. 2014;61(4):353-8. (PMID: 24430729)
      Gynecol Obstet Invest. 2000;49(2):106-9. (PMID: 10671817)
      Diabetes Obes Metab. 2011 Oct;13 Suppl 1:89-94. (PMID: 21824261)
      Diabetes Metab. 2016 Dec;42(6):471-474. (PMID: 27452152)
      Acta Endocrinol (Copenh). 1975 Aug;79(4):709-19. (PMID: 1173969)
      Anal Bioanal Chem. 2017 Oct;409(25):5911-5918. (PMID: 28801845)
      Diabetes Res Clin Pract. 2014 Mar;103(3):412-8. (PMID: 24485857)
      J Clin Invest. 2012 Jan;122(1):4-12. (PMID: 22214853)
      Diabetes Res Clin Pract. 2014 Mar;103(3):341-63. (PMID: 24847517)
      Diabetes. 1991 Dec;40 Suppl 2:39-43. (PMID: 1748264)
      J Diabetes Investig. 2016 May;7(3):324-31. (PMID: 27330717)
      Eur J Endocrinol. 2014 Mar 08;170(4):529-38. (PMID: 24412928)
      Endocr J. 2010;57(11):973-80. (PMID: 20847480)
      Peptides. 2018 Feb;100:54-60. (PMID: 29412832)
      J Diabetes Investig. 2020 Jan;11(1):232-240. (PMID: 31179612)
      Endocr J. 2014;61(4):373-80. (PMID: 24476982)
      Diabetes Care. 1998 Aug;21 Suppl 2:B19-26. (PMID: 9704223)
      Diabetes Care. 2010 Mar;33(3):676-82. (PMID: 20190296)
      Diabetes. 1993 Nov;42(11):1663-72. (PMID: 8405710)
      Diabetes Care. 1999 Sep;22(9):1462-70. (PMID: 10480510)
      Acta Diabetol. 2005 Mar;42(1):31-5. (PMID: 15868111)
      Diabetes Care. 2019 Mar;42(3):372-380. (PMID: 30655380)
      Cell Rep. 2016 Dec 20;17(12):3281-3291. (PMID: 28009296)
      Diabetes Res Clin Pract. 2010 Dec;90(3):339-42. (PMID: 20870307)
      Nat Med. 2010 Jul;16(7):804-8. (PMID: 20581837)
      J Diabetes Investig. 2018 Nov;9(6):1283-1287. (PMID: 29489067)
      Diabetes Care. 2004 Jun;27(6):1487-95. (PMID: 15161807)
      J Diabetes Complications. 2015 Apr;29(3):413-21. (PMID: 25613093)
      Diabetes Obes Metab. 2013 Aug;15(8):713-20. (PMID: 23406269)
      Peptides. 2015 Sep;71:113-20. (PMID: 26206285)
    • Contributed Indexing:
      Keywords: Gestational diabetes; Glucagon; Sandwich enzyme-linked immunosorbent assay
    • Accession Number:
      0 (Biomarkers)
      0 (Blood Glucose)
      0 (Hypoglycemic Agents)
      0 (Insulin)
      9007-92-5 (Glucagon)
    • Publication Date:
      Date Created: 20190611 Date Completed: 20201023 Latest Revision: 20240327
    • Publication Date:
      20240327
    • Accession Number:
      PMC6944843
    • Accession Number:
      10.1111/jdi.13096
    • Accession Number:
      31179612