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Inhibition of PKCβ Improves Glucocorticoid‐Induced Insulin Resistance in Rat Adipocytes
Author(s) -
Kawai Yasunori,
Ishizuka Tatsuo,
Kajita Kazuo,
Miura Atsushi,
Ishizawa Masayoshi,
Natsume Yoshiyuki,
Uno Yoshihiro,
Morita Hiroyuki,
Yasuda Keigo
Publication year - 2002
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540216031
Subject(s) - cycloheximide , medicine , endocrinology , glucocorticoid , insulin resistance , glucocorticoid receptor , dexamethasone , insulin , antagonist , protein kinase c , antiglucocorticoid , insulin receptor , chemistry , biology , receptor , signal transduction , cell culture , microbiology and biotechnology , genetics
Pretreatment with glucocorticoids for 60 min depressed insulin‐stimulated uptake of 2‐[ 3 H] 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 PKC β. The dexamethasone‐mediated inhibitory effect on insulin‐induced 2‐DOG uptake was abrogated in adipocytes overexpressed with dominant‐negative PKC β. These results indicate that PKC βmay play an important role in glucocorticoid‐induced insulin resistance.