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Effect of Coptidis Rhizoma extracts in a water-based solution on insulin resistance in 3T3-L1 adipocytes.

Abstract
The present study was designed to investigate effects and molecular mechanisms of Coptidis Rhizoma extracts (CRE) on the improvement of insulin resistance induced by tumor necrosis factor-α (TNF-α) in adipocytes. We examined whether CRE administration could directly influence the insulin resistance in 3T3-L1 adipocytes. Potential roles of CRE in glucose consumption, mRNA expression of peroxisome proliferators activated receptor (PPAR-γ), expression of insulin receptor substrate-1 (IRS-1) protein, and phosphorylation of IRS-1 Ser307 were also investigated in the present study. Our data demonstrated that TNF-α significantly reduced levels of glucose consumption and IRS-1 protein expression, while TNF-α increased the phosphorylation of IRS-1 Ser307 in adipocytes 24 h after the challenge, suggesting that TNF-α induced a condition with the occurrence of insulin resistance. Those alterations induced by TNF-α were prevented and the mRNA expression of PPAR-γ was up-regulated by the administration of CRE. Thus, our results indicate that CRE can be used to prevent from the TNF-α-induced insulin resistance through PPAR-γ pathways.
AuthorsYi Yuan, Xuhui Wang, Xiaojiong Lu, Yoshinori Marunaka, Xiangdong Wang
JournalBiomedical research (Tokyo, Japan) (Biomed Res) Vol. 35 Issue 5 Pg. 321-7 ( 2014) ISSN: 1880-313X [Electronic] Japan
PMID25355439 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Drugs, Chinese Herbal
  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • PPAR gamma
  • RNA, Messenger
  • Coptidis rhizoma extract
Topics
  • 3T3-L1 Cells
  • Adipocytes (cytology, drug effects, metabolism)
  • Animals
  • Cell Differentiation (drug effects)
  • Coptis chinensis
  • Drugs, Chinese Herbal (pharmacology)
  • Gene Expression
  • Insulin Receptor Substrate Proteins (genetics, metabolism)
  • Insulin Resistance
  • Mice
  • PPAR gamma (genetics, metabolism)
  • Phosphorylation
  • RNA, Messenger (genetics, metabolism)

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