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Title: Plasma gastric inhibitory polypeptide and glucagon-like peptide-1 levels after glucose loading are associated with different factors in Japanese subjects.
Authors: Harada, Norio  kyouindb  KAKEN_id
Hamasaki, Akihiro
Yamane, Shunsuke  kyouindb  KAKEN_id
Muraoka, Atsushi
Joo, Erina
Fujita, Kazuyo
Inagaki, Nobuya  kyouindb  KAKEN_id
Author's alias: 山根, 俊介
稲垣, 暢也
Keywords: Gastric inhibitory polypeptide
Glucagon-like peptide-1
Incretin
Issue Date: 21-Oct-2011
Publisher: wiley
Journal title: Journal of diabetes investigation
Volume: 2
Issue: 3
Start page: 193
End page: 199
Abstract: [Aims/Introduction]: Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are major incretins that potentiate insulin secretion from pancreatic β-cells. The factors responsible for incretin secretion have been reported in Caucasian subjects, but have not been thoroughly evaluated in Japanese subjects. We evaluated the factors associated with incretin secretion during oral glucose tolerance test (OGTT) in Japanese subjects with normal glucose tolerance (NGT). [Materials and Methods]: We measured plasma GIP and GLP-1 levels during OGTT in 17 Japanese NGT subjects and evaluated the factors associated with GIP and GLP-1 secretion using simple and multiple regression analyses. [Results]: GIP secretion (AUC-GIP) was positively associated with body mass index (P < 0.05), and area under the curve (AUC) of C-peptide (P < 0.05) and glucagon (P < 0.01), whereas GLP-1 secretion (AUC-GLP-1) was negatively associated with AUC of plasma glucose (P < 0.05). The insulinogenic index was most strongly associated with GIP secretion (P < 0.05); homeostasis model assessment β-cell was the most the strongly associated factor in GLP-1 secretion (P < 0.05) among the four indices of insulin secretion and insulin sensitivity. [Conclusions]: Several distinct factors might be associated with GIP and GLP-1 secretion during OGTT in Japanese subjects.
Rights: All Journal of Diabetes Investigation articles are published under a Creative Commons License. All Research Councils UK (RCUK) and Wellcome Trust funded authors will be directed to the Creative Commons Attribution license (CC BY) in accordance with funder mandates effective on 1 April 2013. All other authors (non-RCUK and Wellcome Trust authors) will be free to choose from the Creative Commons Attribution Non-Commercial (CC BY NC), and the Attribution-Non-Commercial-NoDerivs (CC BY NC ND)
URI: http://hdl.handle.net/2433/197320
DOI(Published Version): 10.1111/j.2040-1124.2010.00078.x
PubMed ID: 24843483
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