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Articles in PresS, published online ahead of print August 13, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00313.2002
Submitted on July 15, 2002
Accepted on August 3, 2002
1 Department of Cellular and Molecular Medicine, Chiba University, Chiba, Japan; Gene Research Center, Chiba University, Chiba, Japan
2 Department of Cellular and Molecular Medicine, Chiba University, Chiba, Japan
3 Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada
4 Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University, Chiba, Japan
5 Department of Medical Biochemistry, Ehime University School of Medicine, Ehime, Japan
6 Department of Medical Biochemistry, Ehime University School of Medicine, Ehime, Japan; Department of Medicine, Division of Endocrinology, Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: jmrenaud{at}uottawa.ca.
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 is not known, however. We show here that Kir6.2(-/-), mice lacking Kir6.2, the pore-forming subunit of these channels, has no KATP channel activity in their skeletal muscles. 3H-2-deoxyglucose uptake experiment in vivo showed that the basal and insulin-stimulated glucose uptake in skeletal muscles and adipose tissues of Kir6.2(-/-) mice are enhanced, compared to 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(-/-) EDL 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.
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