MISC

2006年3月

Protein kinase C attenuates beta-adrenergic receptor-mediated lipolysis, probably through inhibition of the beta(1)-adrenergic receptor system

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
  • J Nakamura

447
1
開始ページ
1
終了ページ
10
記述言語
英語
掲載種別
DOI
10.1016/j.abb.2006.01.011
出版者・発行元
ELSEVIER SCIENCE INC

Lipolysis in rat white adipocytes is stimulated by P-adrenergic agonists. Phorbol 12-myristate 13-acetate (PMA) attenuated the receptor-mediated lipolysis by causing a shift of the dose-response curve to the higher concentrations of norepinephrine and isoproterenol. Although the adipocytes possess beta(-)(1), beta(-)(2), and beta(3)-adrenergic receptor Subtypes, the effect of PMA was observed only when a beta(1)-agonist (dobutamine) was used. No lipolysis-attenuating effect of PMA was found when cells were exposed to a beta(2)-agonist (procaterol) and beta(3)-agonists (BRL 37344 and CL 316243), or to forskolin and 8-brorno cAMP. CGP 20712A (PI-antagonist) efficiently inhibited lipolysis by norepinephrine, isoproterenol, and dobutamine, but did not affect lipolysis by the beta(2)- and beta(3)-agonists. ICI 118551 (beta(2)-antagonist) had no significant effect on lipolysis by the beta-agonists examined. CGP 20712A abolished the lipolysis-attenuating effect of PMA, but ICI 118551 did not. The protein kinase C (PKC) inhibitors. GF 109203X or Go 6976, suppressed the effect of PMA. Pretreatment of adipocytes with PMA for 6h caused downregulation of conventional and novel PKCs in association with a decrease in the lipolysis-attenuating effect of PMA. These results indicate that conventional and novel PKCs attenuate lipolysis mediated by beta-adrenergic receptors, probably through inhibition of the beta(1)-adrenergic receptor system. (c) 2006 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.abb.2006.01.011
CiNii Articles
http://ci.nii.ac.jp/naid/80019273391
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/16500613
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000236052300001&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.abb.2006.01.011
  • ISSN : 0003-9861
  • CiNii Articles ID : 80019273391
  • PubMed ID : 16500613
  • Web of Science ID : WOS:000236052300001

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