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Endocrinology Vol. 142, No. 4 1595-1605
Copyright © 2001 by The Endocrine Society

ARTICLES

Rosiglitazone, Insulin Treatment, and Fasting Correct Defective Activation of Protein Kinase C-{zeta}/{lambda} by Insulin in Vastus Lateralis Muscles and Adipocytes of Diabetic Rats1

Yoshinori Kanoh, Gautam Bandyopadhyay, Mini P. Sajan, Mary L. Standaert and Robert V. Farese

J. A. Haley Veterans Hospital Research Service and Department of Internal Medicine, University of South Florida College of Medicine Tampa, Florida 33612

Address all correspondence and requests for reprints to: Robert V. Farese, M.D., Research Service (VAR 151), J. A. Haley Veterans Hospital, 13000 Bruce B. Downs Boulevard, Tampa, Florida 33612. E-mail: rfarese{at}com1.med.usf.edu

Atypical protein kinases C (PKCs), {zeta} and {lambda}, and protein kinase B (PKB) are thought to function downstream of phosphatidylinositol 3-kinase (PI 3-kinase) and regulate glucose transport during insulin action in skeletal muscle and adipocytes. Insulin-stimulated glucose transport is defective in type II diabetes mellitus, and this defect is ameliorated by thiazolidinediones and lowering of blood glucose by chronic insulin therapy or short-term fasting. Presently, we evaluated the effects of these insulin-sensitizing modalities on the activation of insulin receptor substrate-1 (IRS-1)-dependent PI 3-kinase, PKC-{zeta}/{lambda}, and PKB in vastus lateralis skeletal muscles and adipocytes of nondiabetic and Goto-Kakizaki (GK) diabetic rats. Insulin provoked rapid increases in the activity of PI 3-kinase, PKC-{zeta}/{lambda}, and PKB in muscles and adipocytes of nondiabetic rats, but increases in IRS-1-dependent PI 3-kinase and PKC-{zeta}/{lambda}, but not PKB, activity were substantially diminished in GK muscles and adipocytes. Rosiglitazone treatment for 10–14 days, 10-day insulin treatment, and 60-h fasting reversed defects in PKC-{zeta}/{lambda} activation in GK muscles and adipocytes and increased glucose transport in GK adipocytes, without necessarily increasing IRS-1-dependent PI 3-kinase or PKB activation. Our findings suggest that insulin-sensitizing modalities, viz. thiazolidinediones, chronic insulin treatment, and short-term fasting, similarly improve defects in insulin-stimulated glucose transport at least partly by correcting defects in insulin-induced activation of PKC-{zeta}/{lambda}.




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