کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2533236 | 1559041 | 2011 | 6 صفحه PDF | دانلود رایگان |
Although nonalcoholic steatohepatitis (NASH) is associated with insulin resistance partly due to reduced levels of circulating adiponectin, the role of adiponectin receptors including adiponectin receptor 1 and adiponectin receptor 2 in adipose tissues in NASH remains controversial. The present study showed that there was a marked decline in adiponectin receptor 1 and adiponectin receptor 2 expressions in liver and visceral fat, and these expressions were elevated in muscle of NASH rats 12 weeks after oral administration of a high-fat diet. An 8-week continuous treatment with rosiglitazone, a peroxisome proliferator-activated receptors γ (PPAR γ) agonist improved the histological lesions markedly in liver of NASH rats, and concurrently increased mRNA and protein expressions of adiponectin receptor 1 and adiponectin receptor 2 in liver and visceral fat, with down-regulation of the two receptors in muscle. There was a negative correlation between the ratio of adiponectin receptors/β-actin protein and serum TNF-α in the liver and visceral fat, and a positive correlation in muscle. Additionally, rosiglitazone increased circulating adiponectin, which was negatively correlated with serum TNF-α. These results indicated that rosiglitazone improved NASH by directly modulating adiponectin receptor 1 and adiponectin receptor 2 in various adipose tissues, or indirectly possibly via decreasing serum TNF-α.
Journal: European Journal of Pharmacology - Volume 650, Issue 1, 10 January 2011, Pages 384–389