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Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice.

Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Research Abstract Details 

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  • Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Abstract Text:

    hiroki fujitaHiroki Fujita,masafumi kakeiMasafumi Kakei,hiromi fujishimaHiromi Fujishima,tsukasa moriiTsukasa Morii,yuichiro yamadaYuichiro Yamada,zhonghua qiZhonghua Qi,matthew d breyerMatthew D Breyer,hiroki fujitaHiroki Fujita,masafumi kakeiMasafumi Kakei,hiromi fujishimaHiromi Fujishima,tsukasa moriiTsukasa Morii,yuichiro yamadaYuichiro Yamada,zhonghua qiZhonghua Qi,matthew d breyerMatthew D Breyer,hiroki fujitaHiroki Fujita,masafumi kakeiMasafumi Kakei,hiromi fujishimaHiromi Fujishima,tsukasa moriiTsukasa Morii,yuichiro yamadaYuichiro Yamada,zhonghua qiZhonghua Qi,matthew d breyerMatthew D Breyer,

    Previous studies have shown that Prostaglandin E(2) (PGE(2)) inhibits glucose-stimulated insulin secretion. However, the role of cyclooxygenase (COX)-1 vs. COX-2 derived PGE(2) production in glucose-stimulated insulin secretion remains poorly understood. Here we investigated the expression of COX-1 and COX-2 in pancreatic islets and the effect of selective inhibition of COX-1 and COX-2 on glucose-stimulated insulin secretion using C57BL/6 (B6) mice. Although immunofluorescence histochemistry showed the constitutive expression of both COX-1 and COX-2 in B6 mouse pancreatic islets, insulin secretion and hyperglycemia after glucose loading were ameliorated in B6 mice treated with selective COX-2 inhibitor (SC58236) for 18 weeks. Interestingly, incubation with selective COX-2 inhibitor for 24h led to a reduction in PGE(2) production in pancreatic islets isolated from B6 mice. In addition, selective COX-2 inhibition enhanced insulin secretion from the isolated islets. These results collectively suggest that selective inhibition of COX-2 enhances glucose-stimulated insulin secretion through a reduction in PGE(2) production in pancreatic islets.

    Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Publishing Authors By Initials

    h fujitaH Fujita,m kakeiM Kakei,h fujishimaH Fujishima,t moriiT Morii,y yamadaY Yamada,z qiZ Qi,md breyerMD Breyer,h fujitaH Fujita,m kakeiM Kakei,h fujishimaH Fujishima,t moriiT Morii,y yamadaY Yamada,z qiZ Qi,md breyerMD Breyer,h fujitaH Fujita,m kakeiM Kakei,h fujishimaH Fujishima,t moriiT Morii,y yamadaY Yamada,z qiZ Qi,md breyerMD Breyer,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

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    Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Biochemical and biophysical research communication

    VOLUME: 363

    Page Numbers: 37-43

    Journal Abbreviation: Biochem. Biophys. Res. Commun.

    ISSN: 0006-291X

    DAY: 27

    MONTH: 08

    YEAR: 2007

    Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 372516

    Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice. Information

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    Grant and Affiliation Information for Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice.

    AFFILIATION: Division of Endocrinology, Metabolism and Geriatric Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan. hirofuji@gipc.akita-u.ac.jp

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: DK74116

    ACRONYM: DK

    MEDLINETA: Biochem Biophys Res Commun

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