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

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)329-332
Number of pages4
JournalFEBS Letters
Volume371
Issue number3
DOIs
Publication statusPublished - 1995 Sep 11
Externally publishedYes

Keywords

  • Antisense mRNA
  • Glucokinase
  • Glucose homeostasis
  • Transgenic mouse

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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