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

doi:10.1016/0014-5793(95)00932-Y

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

MED - Medical Sciences

Research output: Contribution to journal › Article › peer-review

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 language	English
Pages (from-to)	329-332
Number of pages	4
Journal	FEBS Letters
Volume	371
Issue number	3
DOIs	https://doi.org/10.1016/0014-5793(95)00932-Y
Publication status	Published - 1995 Sept 11

Keywords

Antisense mRNA
Glucokinase
Glucose homeostasis
Transgenic mouse

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10.1016/0014-5793(95)00932-Y

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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.",

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T1 - Inhibition of pancreatic β-cell glucokinase by antisense RNA expression in transgenic mice

T2 - mouse strain-dependent alteration of glucose tolerance

AU - Ishihara, Hisamitsu

AU - Tashiro, Fumi

AU - Ikuta, Koichi

AU - Asano, Tomoichiro

AU - Katagiri, Hideki

AU - Inukai, Koichi

AU - Kikuchi, Masatoshi

AU - Yazaki, Yoshio

AU - Oka, Yoshitomo

AU - Miyazaki, Jun ichi

PY - 1995/9/11

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N2 - 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.

AB - 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.

KW - Antisense mRNA

KW - Glucokinase

KW - Glucose homeostasis

KW - Transgenic mouse

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

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Keywords

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