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1 Department of Cellular and Molecular Medicine, Graduate School of Medicine, 3 Research Center for Pathogenic Fungi and Microbial Toxicoses, and 5 Gene Research Center, Chiba University, Chiba 260-8670; 4 Department of Medical Biochemistry, Ehime University School of Medicine, Ehime 791-0295, Japan; and 2 Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada
ATP-sensitive potassium
(KATP) channels are known to be critical in the control of
both insulin and glucagon secretion, the major hormones in the
maintenance of glucose homeostasis. The involvement of KATP
channels in glucose uptake in the target tissues of insulin, however,
is not known. We show here that Kir6.2(
/) mice lacking Kir6.2, the
pore-forming subunit of these channels, have no KATP
channel activity in their skeletal muscles. A
2-deoxy-[3H]glucose uptake experiment in vivo showed that
the basal and insulin-stimulated glucose uptake in skeletal muscles and
adipose tissues of Kir6.2(/) mice is enhanced compared with that in wild-type (WT) mice. In addition, in vitro measurement of glucose uptake indicates that disruption of the channel increases the basal
glucose uptake in Kir6.2(/) extensor digitorum longus and the
insulin-stimulated glucose uptake in Kir6.2(/) soleus muscle. In
contrast, glucose uptake in adipose tissue, measured in vitro, was
similar in Kir6.2(/) and WT mice, suggesting that the increase in
glucose uptake in Kir6.2(/) adipocytes is mediated by altered
extracellular hormonal or neuronal signals altered by disruption of the
KATP channels.
Kir6.2; SUR2; sulfonylurea; insulin; knockout mice
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