MISC

2001年3月

Glucocorticoid-induced insulin resistance associates with activation of protein kinase C isoforms

CELLULAR SIGNALLING
  • K Kajita
  • ,
  • T Ishizuka
  • ,
  • A Miura
  • ,
  • Y Kanoh
  • ,
  • M Ishizawa
  • ,
  • M Kimura
  • ,
  • N Muto
  • ,
  • K Yasuda

13
3
開始ページ
169
終了ページ
175
記述言語
英語
掲載種別
DOI
10.1016/S0898-6568(01)00143-7
出版者・発行元
ELSEVIER SCIENCE INC

We studied glucocorticoid-induced insulin resistance and possible role of protein kinase C (PKC). Pretreatment with dexamethasone, prednisolone and corticosterone for 60 min decreased insulin-induced [H-3] 2-deoxyglucose (DOG) uptake in isolated rat adipocytes. Preincubation with Go6976, LY379196 or myristoylated PKC pseudosubstrate. conventional PKC inhibitor, but not cycloheximide or RU38486, recovered dexamethasone-induced insulin resistance. Dexamethasone activated immunoprecipitates with anti-PKC alpha, beta, and zeta antibodies. PKC zeta activity in adipocytes increased to 163%. and 264% from basal level (100%) with dexamethasone and insulin treatment, respectively. Dexamethasone provoked redistribution of both PKC beta and zeta from the cytosol to the membrane. These results indicate that dexamethasone activates both conventional and atypical PKC. However, conventional PKC is more important in glucocorticoid-induced insulin resistance. (C) 2001 Elsevier Science Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/S0898-6568(01)00143-7
CiNii Articles
http://ci.nii.ac.jp/naid/80012366671
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/11282455
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000167933500003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/S0898-6568(01)00143-7
  • ISSN : 0898-6568
  • CiNii Articles ID : 80012366671
  • PubMed ID : 11282455
  • Web of Science ID : WOS:000167933500003

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