Inhibition of PKCbeta improves glucocorticoid-induced insulin resistance in rat adipocytes |
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Authors: | Kawai Yasunori Ishizuka Tatsuo Kajita Kazuo Miura Atsushi Ishizawa Masayoshi Natsume Yoshiyuki Uno Yoshihiro Morita Hiroyuki Yasuda Keigo |
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Affiliation: | The Third Department of Internal Medicine, Gifu University School of Medicine, Tsukasa-machi 40, Gifu 500, Japan. |
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Abstract: | Pretreatment with glucocorticoids for 60 min depressed insulin-stimulated uptake of 2-[3H] deoxyglucose (2-DOG), an effect that neither cycloheximide, an inhibitor of protein synthesis, nor RU38486, a glucocorticoid receptor antagonist, could restore. Preincubation with conventional PKC inhibitors restored dexamethasone-induced insulin resistance. We also examined the dexamethasone-mediated inhibitory effect on insulin-induced 2-DOG uptake in adipocytes overexpressed with wild-type and dominant negative forms of PKCbeta. The dexamethasone-mediated inhibitory effect on insulin-induced 2-DOG uptake was abrogated in adipocytes overexpressed with dominant-negative PKCbeta. These results indicate that PKCbeta may play an important role in glucocorticoid-induced insulin resistance. |
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