Inhibition of pancreatic β-cell glucokinase by antisense RNA expression in transgenic mice: mouse strain-dependent alteration of glucose tolerance

Hisamitsu Ishihara, Fumi Tashiro, Koichi Ikuta, Tomoichiro Asano, Hideki Katagiri, Koichi Inukai, Masatoshi Kikuchi, Yoshio Yazaki, Yoshitomo Oka, Jun ichi Miyazaki

研究成果: Article査読

21 被引用数 (Scopus)

抄録

We have generated transgenic mice, in either C57BL/6 or C3H background, expressing antisense glucokinase mRNA in β-cells. The glucose phosphorylating activity at 60 mM glucose in transgenic islets was significantly lower than that in controls, and the insulin secretory response to glucose was lower in transgenic islets than in those of controls in both strains. Following i.p. glucose challenge, higher blood glucose levels were observed in transgenic mice than in controls in the C57BL/6 nut not the C3H background. These data suggest that a β-cell secretory defect, in combination with other undefined genetic factors, causes impaired glucose homeostasis in mice.

本文言語English
ページ(範囲)329-332
ページ数4
ジャーナルFEBS Letters
371
3
DOI
出版ステータスPublished - 1995 9月 11
外部発表はい

ASJC Scopus subject areas

  • 生物理学
  • 構造生物学
  • 生化学
  • 分子生物学
  • 遺伝学
  • 細胞生物学

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