当前位置： SCI文献检索 > JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION期刊下所有文献 > The inhibitory effects of PKCθ on adiponectin expression is mediated by ERK in 3T3-L1 adipocytes.

The inhibitory effects of PKCθ on adiponectin expression is mediated by ERK in 3T3-L1 adipocytes.

Abstract：

:The research suggests that adiponectin plays an important role in sensitizing insulin action. It is interesting to find that the lower levels of adiponectin exist in the plasma of obese and Type 2 diabetes subjects and in the adipose tissue of obese, db/db mice, and insulin-resistant individuals. However, the underlying mechanism by which adiponectin expression is inhibited remains largely unknown. In this study, we reported that adipogenesis was inhibited by the stable over-expression of protein kinase C θ (PKCθ) in 3T3-L1 pre - adipocytes. The prolonged treatment of mature 3T3-L1 adipocytes with palmitate, a kind of saturated free fatty acid, reduced adiponectin expression at both mRNA level and protein level, accompanied with the enhanced phosphorylation of PKCθ and extracellular signal-regulated kinase (ERK), and the impaired expression of peroxisome proliferator-activated receptor γ2 (PPARγ2) mRNA. Either PD98059, an ERK inhibitor or PKCθ pseudosubstrate, a specific PKCθ inhibitor, restored palmiate-inhibited PPARγ2 mRNA expression and subsequent adiponectin expression. In addition, the over-expression or activation of PKCθ resulted in the enhanced phosphorylation of ERK in the mature 3T3-L1 adipocytes. PKCθ pseudosubstrate significantly reduced the phorbol 3-myristate 12-acetate (PMA)-induced phosphorylation of ERK. The data suggested that PKCθ-dependent activity of ERK resulted in the impaired expression of PPARγ2 mRNA leading to the reduction of adiponectin expression in the mature 3T3-L1 adipocytes.

journal_name

J Endocrinol Invest

journal_title

Journal of endocrinological investigation

authors

Sun S,Liu Y,Lu J,Omar A,Sun S,Bi Y,Wang C

doi

10.1007/BF03346688

subject

Has Abstract

pub_date

2011-01-01 00:00:00

pages

8-15

issue

1

eissn

0391-4097

issn

1720-8386

pii

6948

journal_volume

34

pub_type

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