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Inhibition of pancreatic β‐cell glucokinase by antisense RNA expression in transgenic mice: mouse strain‐dependent alteration of glucose tolerance
Author(s) -
Hideharu Ishihara,
Fumi Tashiro,
Koichi Ikuta,
Tomohiko Asano,
Hideki Katagiri,
Koichi Inukai,
Masatoshi Kikuchi,
Yoshio Yazaki,
Yoshitomo Oka,
Junichi Miyazaki
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00932-y
Subject(s) - glucokinase , genetically modified mouse , transgene , glucose homeostasis , islet , biology , medicine , endocrinology , antisense rna , pancreatic islets , insulin , rna , biochemistry , gene , insulin resistance
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.