Inhibition of pancreatic β-cell glucokinase by antisense RNA expression in transgenic mice: mouse strain-dependent alteration of glucose tolerance
H Ishihara, F Tashiro, K Ikuta, T Asano, H Katagiri… - FEBS letters, 1995 - Elsevier
H Ishihara, F Tashiro, K Ikuta, T Asano, H Katagiri, K Inukai, M Kikuchi, Y Yazaki, Y Oka…
FEBS letters, 1995•ElsevierWe 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 ip 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 …
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 ip 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 …
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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