期刊
PPAR RESEARCH
卷 2012, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2012/107434
关键词
-
资金
- National Commission for Scientific and Technological Research (FONDECYT) (Chile) [1120034]
Nonalcoholic fatty liver disease in human obesity is characterized by the multifactorial nature of the underlying pathogenic mechanisms, which include misregulation of PPARs signaling. Liver PPAR-alpha downregulation with parallel PPAR-gamma and SREBP-1c up-regulation may trigger major metabolic disturbances between de novo lipogenesis and fatty acid oxidation favouring the former, in association with the onset of steatosis in obesity-induced oxidative stress and related long-chain polyunsaturated fatty acid n-3 (LCPUFA n-3) depletion, insulin resistance, hypoadiponectinemia, and endoplasmic reticulum stress. Considering that antisteatotic strategies targeting PPAR-alpha revealed that fibrates have poor effectiveness, thiazolidinediones have weight gain limitations, and dual PPAR-alpha/gamma agonists have safety concerns, supplementation with LCPUFA n-3 appears as a promising alternative, which achieves both significant reduction in liver steatosis scores and a positive anti-inflammatory outcome. This latter aspect is of importance as PPAR-alpha downregulation associated with LCPUFA n-3 depletion may play a role in increasing the DNA binding capacity of proinflammatory factors, NF-kappa B and AP-1, thus constituting one of the major mechanisms for the progression of steatosis to steatohepatitis.
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