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Title: Mechanisms of fat-induced gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide secretion from K cells
Authors: Yamane, Shunsuke  kyouindb  KAKEN_id
Harada, Norio  kyouindb  KAKEN_id
Inagaki, Nobuya  kyouindb  KAKEN_id
Author's alias: 山根, 俊介
原田, 範雄
稲垣, 暢也
Keywords: Fatty acid-binding protein 5
G protein-coupled receptor 120
Regulatory factor X6
Issue Date: Apr-2016
Publisher: Asian Association of the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd
Journal title: Journal of Diabetes Investigation
Volume: 7
Issue: S1
Start page: 20
End page: 26
Abstract: Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP) is one of the incretins, which are gastrointestinal hormones released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion. Single fat ingestion stimulates GIP secretion from enteroendocrine K cells; chronic high-fat diet (HFD) loading enhances GIP secretion and induces obesity in mice in a GIP-dependent manner. However, the mechanisms of GIP secretion from K cells in response to fat ingestion and GIP hypersecretion in HFD-induced obesity are not well understood. We generated GIP-green fluorescent protein knock-in (GIPgfp/+) mice, in which K cells are labeled by enhanced GIP-green fluorescent protein. Microarray analysis of isolated K cells from GIPgfp/+ mice showed that both fatty acid-binding protein 5 and G protein-coupled receptor 120 are highly expressed in K cells. Single oral administration of fat resulted in significant reduction of GIP secretion in both fatty acid-binding protein 5- and G protein-coupled receptor 120-deficient mice, showing that fatty acid-binding protein 5 and G protein-coupled receptor 120 are involved in acute fat-induced GIP secretion. Furthermore, the transcriptional factor, regulatory factor X6 (Rfx6), is highly expressed in K cells. In vitro experiments using the mouse enteroendocrine cell line, STC-1, showed that GIP messenger ribonucleic acid levels are upregulated by Rfx6. Expression levels of Rfx6 messenger ribonucleic acid as well as that of GIP messenger ribonucleic acid were augmented in the K cells of HFD-induced obese mice, in which GIP content in the small intestine is increased compared with that in lean mice fed a control diet. These results suggest that Rfx6 is involved in hypersecretion of GIP in HFD-induced obese conditions by increasing GIP gene expression.
Rights: © 2016 The Authors. Journal of Diabetes Investigation published by Asian Association of the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
DOI(Published Version): 10.1111/jdi.12467
Appears in Collections:Journal Articles

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