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.
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Authors | Yi Yuan, Xuhui Wang, Xiaojiong Lu, Yoshinori Marunaka, Xiangdong Wang |
Journal | Biomedical research (Tokyo, Japan)
(Biomed Res)
Vol. 35
Issue 5
Pg. 321-7
( 2014)
ISSN: 1880-313X [Electronic] Japan |
PMID | 25355439
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Drugs, Chinese Herbal
- Insulin Receptor Substrate Proteins
- Irs1 protein, mouse
- PPAR gamma
- RNA, Messenger
- Coptidis rhizoma extract
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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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