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Destruction of pancreatic β-cells by transgenic induction of prostaglandin e2 in the islets
https://doi.org/10.24517/00027354
https://doi.org/10.24517/000273547b42a0ea-a3a0-47f6-9354-2128d1a73617
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-OOSHIMA-H-03.pdf (860.9 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-10-05 | |||||||||
| タイトル | ||||||||||
| タイトル | Destruction of pancreatic β-cells by transgenic induction of prostaglandin e2 in the islets | |||||||||
| 言語 | ||||||||||
| 言語 | eng | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | journal article | |||||||||
| ID登録 | ||||||||||
| ID登録 | 10.24517/00027354 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Oshima, Hiroko
× Oshima, Hiroko× Taketo, Makoto Mark× Oshima, Masanobu |
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| 著者別表示 |
大島, 浩子
× 大島, 浩子
× 大島, 正伸
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学がん研究所附属がん幹細胞研究センター | |||||||||
| 書誌情報 |
Journal of Biological Chemistry 巻 281, 号 39, p. 29330-29336, 発行日 2006-09-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 0021-9258 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isVersionOf | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | https://doi.org/10.1074/jbc.m602424200 | |||||||||
| 出版者 | ||||||||||
| 出版者 | American Society of Biochemistry and Molecular Biology | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Type 2 diabetes mellitus is characterized by insulin resistance of peripheral tissues and dysfunction of pancreatic β-cells. Furthermore, the number of pancreatic β-cells decreases as a secondary effect of advanced type 2 diabetes, although the molecular mechanism has not been elucidated. Recently, it has been shown that hyperglycemic conditions induce the expression of cyclooxygenase-2 in pancreatic islets and increase the downstream product prostaglandin E2 (PGE2). To investigate whether high glucose-induced PGE2 has an adverse effect on pancreatic β-cells, we generated transgenic mice (RIP-C2mE) that express cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in their β-cells using the rat insulin-2 gene promoter (RIP). The homozygous RIP-C2mE (Tg/Tg) mice showed severe hyperglycemia from six weeks of age. Although the heterozygous RIP-C2mE (Tg/-) mice showed normal blood glucose levels throughout their lifetime, this level increased significantly compared with that of wild-type mice when glucose was loaded. The relative number of β-cells to the total islet cell number was reduced to 54 and 14% in the RIP-C2mE (Tg/-) and (Tg/Tg) mice, respectively, whereas that in the wild-type mice was 84%. Importantly, the proliferation rate in the islets of the RIP-C2mE (Tg/Tg) mice at four weeks of age decreased significantly in comparison to that in the wild-type mice. Because β-cells replicate not only during the postnatal period but also in the adult pancreas at a basal level, it is possible that increased PGE2 signaling thus contributes to the reduction of the pancreatic β-cell mass through inhibition of proliferation, thereby aggravating diabetes further. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc. | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
