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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Chen, Dai Kou, Xin-hui Lu, Yi Ye, Jian-lin Zhu, Mei-feng Song, Hui-zhu Yue, Lin-feng |
| Description | Author Affiliation: Kou XH ( Department of Pharmacy, Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi, China. xinhuikou1980@yahoo.com) |
| Abstract | BACKGROUND AND PURPOSE: The amelioration of insulin resistance by bilobetin is closely related to its hypolipidaemic effect. The aim of the present study was to determine the insulin-sensitizing mechanism of bilobetin by elucidating its effect on lipid metabolism. EXPERIMENTAL APPROACH: Rats fed a high-fat diet were treated with bilobetin for either 4 or 14 days before applying a hyperinsulinaemic-euglycaemic clamp. Triglyceride and fatty acids labelled with radioactive isotopes were used to track the transportation and the fate of lipids in tissues. The activity of lipid metabolism-related enzymes and ß-oxidation rate were measured. Western blot was used to investigate the phosphorylation, translocation and expression of PPAR in several tissues and cultured cells. The location of amino acid residues subjected to phosphorylation in PPAR was also studied. KEY RESULTS: Bilobetin ameliorated insulin resistance, increased the hepatic uptake and oxidation of lipids, reduced very-low-density lipoprotein triglyceride secretion and blood triglyceride levels, enhanced the expression and activity of enzymes involved in ß-oxidation and attenuated the accumulation of triglycerides and their metabolites in tissues. Bilobetin also increased the phosphorylation, nuclear translocation and activity of PPAR accompanied by elevated cAMP level and PKA activity. Threonine-129-alanine and/or serine-163-alanine mutations on the PPAR genes and PKA inhibitors prevented the effects of bilobetin on PPAR . However, cells overexpressing PKA appeared to stimulate the phosphorylation, nuclear translocation and activity of PPAR . CONCLUSIONS AND IMPLICATIONS: Bilobetin treatment ameliorates hyperlipidaemia, lipotoxicity and insulin resistance in rats by stimulating PPAR -mediated lipid catabolism. PKA activation is crucial for this process. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 8 |
| Volume Number | 165 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2012-04-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Cyclic AMP-Dependent Protein Kinases Metabolism Flavonoids Therapeutic Use Hypolipidemic Agents Insulin Resistance PPAR Alpha Alanine Transaminase Blood Animals Aspartate Aminotransferases Cells, Cultured Diet, High-Fat Pharmacology Hepatocytes Drug Effects Hyperlipidemias Drug Therapy Lipid Metabolism Liver Muscle, Skeletal Rats, Sprague-Dawley |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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