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Articles in PresS, published online ahead of print March 12, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00457.2001
Submitted on October 11, 2001
Accepted on February 27, 2002
1 Third Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan
2 Division of Molecular Metabolism and Diabetes, Department of Internal Medicine, Tohoku University Graduate School of Medicine, Seiryo-machi, Sendai, Japan
3 Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan
4 Third Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan; Division of Molecular Metabolism and Diabetes, Department of Internal Medicine, Tohoku University Graduate School of Medicine, Seiryo-machi, Sendai, Japan
5 Department of Molecular Biology, Yokohama City University School of Medicine, Kanazawa-ku, Yokohama, Japan
* To whom correspondence should be addressed. E-mail: oka{at}int3.med.tohoku.ac.jp.
To elucidate the involvement of protein kinase C (PKC) isoforms in insulin-induced and phorbol ester-induced glucose transport, we expressed several PKC isoforms, conventional PKC
, novel PKC
, and atypical PKC isoforms of PKC
and PKC
, and their mutants in 3T3-L1 adipocytes using adenovirus-mediated gene transduction system. Endogenous expression and the activities of PKC and PKC/, but not of PKC, were detected in 3T3-L1 adipocytes. Overexpression of each wild-type PKC isoform induced a large amount of PKC activity in 3T3-L1 adipocytes. Phorbol 12-myristrate 13-acetate (PMA) activated PKC and exogenous PKC, but not atypical PKC/. Insulin also activated the overexpressed PKCd but not PKCa. Expression of the wild-type PKC or PKC resulted in significant increases in glucose transport activity in the basal and PMA-stimulated states. Dominant-negative PKC expression, which inhibited the PMA activation of PKC, decreased in PMA-stimulated glucose transport. Glucose transport activity in the insulin-stimulated state was increased by the expression of PKC but not of PKC. These findings demonstrate that both conventional and novel PKC isoforms are involved in PMA-stimulated glucose transport and that other novel PKC isoforms could participate in PMA-stimulated and insulin-stimulated glucose transport. Atypical PKC/ was not significantly activated by insulin and expression of the wild-type, constitutively active and dominant-negative mutants of atypical PKC did not affect either basal or insulin-stimulated glucose transport. Thus, atypical PKC enzymes do not play a major role in insulin-stimulated glucose transport in 3T3-L1 adipocytes.
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