Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients

Daisuke Yabe, Akira Kuroe, Koin Watanabe, Masahiro Iwasaki, Akihiro Hamasaki, Yoshiyuki Hamamoto, Norio Harada, Shunsuke Yamane, Soushou Lee, Kenta Murotani, Carolyn F Deacon, Jens Juul Holst, Tsutomu Hirano, Nobuya Inagaki, Takeshi Kurose, Yutaka Seino

30 Citations (Scopus)

Abstract

AIMS: Hypersecretion of glucagon and reduced insulin secretion both contribute to hyperglycemia in type 2 diabetes (T2DM). However, the relative contributions of impaired glucagon and insulin secretions in glucose excursions at the various stages of T2DM development remain to be determined.

METHODS: The responses of glucagon and insulin as well as those of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were examined before and after ingestion of glucose or mixed meal in Japanese subjects with normal or impaired glucose tolerance (NGT and IGT) and in non-obese, untreated T2DM of short duration.

RESULTS: In OGTT, T2DM showed a rise in glucagon at 0-30min, unlike NGT and IGT, along with reduced insulin. In MTT, all three groups showed a rise in glucagon at 0-30min, with that in T2DM being highest, while T2DM showed a significant reduction in insulin. Linear regression analyses revealed that glucose area under the curve (AUC)0-120 min was associated with glucagon-AUC0-30 min and insulin-AUC0-30 min in both OGTT and MTT. Total and biologically intact GIP and GLP-1 levels were similar among the three groups.

CONCLUSIONS: Disordered early phase insulin and glucagon secretions but not incretin secretion are involved in hyperglycemia after ingestion of nutrients in T2DM of even a short duration.

Original languageEnglish
JournalJournal of Diabetes and its Complications
Volume29
Pages (from-to)413-421
Number of pages9
ISSN1056-8727
DOIs
Publication statusPublished - 1 Apr 2015

Fingerprint

Dive into the research topics of 'Early phase glucagon and insulin secretory abnormalities, but not incretin secretion, are similarly responsible for hyperglycemia after ingestion of nutrients'. Together they form a unique fingerprint.

Cite this