A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice.

A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice. Research Abstract Details 

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A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice. Abstract Text:

Norio Harada,Yuichiro Yamada,Katsushi Tsukiyama,Chizumi Yamada,Yasuhiko Nakamura,Eri Mukai,Akihiro Hamasaki,Xibao Liu,Kentaro Toyoda,Yutaka Seino,Nobuya Inagaki,Norio Harada,Yuichiro Yamada,Katsushi Tsukiyama,Chizumi Yamada,Yasuhiko Nakamura,Eri Mukai,Akihiro Hamasaki,Xibao Liu,Kentaro Toyoda,Yutaka Seino,Nobuya Inagaki,

Gastric inhibitory polypeptide (GIP) is an incretin that potentiates insulin secretion from pancreatic beta-cells by binding to GIP receptor (GIPR) and subsequently increasing the level of intracellular adenosine 3',5'-cyclic monophosphate (cAMP). We have identified a novel GIPR splice variant in mouse beta-cells that retains intron 8, resulting in a COOH-terminal truncated form (truncated GIPR). This isoform was coexpressed with full-length GIPR (wild-type GIPR) in normal GIPR-expressing tissues. In an experiment using cells transfected with both GIPRs, truncated GIPR did not lead to cAMP production induced by GIP but inhibited GIP-induced cAMP production through wild-type GIPR (n = 3-4, P < 0.05). Wild-type GIPR was normally located on the cell surface, but its expression was decreased in the presence of truncated GIPR, suggesting a dominant negative effect of truncated GIPR against wild-type GIPR. The functional relevance of truncated GIPR in vivo was investigated. In high-fat diet-fed obese mice (HFD mice), blood glucose levels were maintained by compensatory increased insulin secretion (n = 8, P < 0.05), and cAMP production (n = 6, P < 0.01) and insulin secretion (n = 10, P < 0.05) induced by GIP were significantly increased in isolated islets, suggesting hypersensitivity of the GIPR. Total GIPR mRNA expression was not increased in the islets of HFD mice, but the expression ratio of truncated GIPR to total GIPR was reduced by 32% compared with that of control mice (n = 6, P < 0.05). These results indicate that a relative reduction of truncated GIPR expression may be involved in hypersensitivity of GIPR and hyperinsulinemia in diet-induced obese mice.

A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice. Publishing Authors By Initials

N Harada,Y Yamada,K Tsukiyama,C Yamada,Y Nakamura,E Mukai,A Hamasaki,X Liu,K Toyoda,Y Seino,N Inagaki,N Harada,Y Yamada,K Tsukiyama,C Yamada,Y Nakamura,E Mukai,A Hamasaki,X Liu,K Toyoda,Y Seino,N Inagaki,

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A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: American journal of physiology. Endocrinology and

VOLUME: 294

Page Numbers: E61-8

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 30

MONTH: 10

YEAR: 2007

A novel GIP receptor splice variant influences GIP sensitivity of pancreatic -cells in obese mice. Information

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LANGUAGE: eng

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AFFILIATION: Dept. of Internal Medicine, Div. of Endocrinology, Diabetes, and Geriatric Medicine, Akita University School of Medicine, 1-1-1, Hondo, Akita 010-8543, Japan. yamada@gipc.akita-u.ac.jp).

Country: United States

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MEDLINETA: Am J Physiol Endocrinol Metab

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