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PPARs and nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) encompasses a range of liver pathology ranging from simple steatosis to varying degrees of inflammation, hepatocyte injury and fibrosis. Without intervention it can progress to end-stage liver disease and hepatocellular carcinoma. Given its close association...

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Bibliographic Details
Published in:Biochimie 2017-05, Vol.136, p.65-74
Main Authors: Liss, Kim H.H., Finck, Brian N.
Format: Article
Language:English
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Summary:Nonalcoholic fatty liver disease (NAFLD) encompasses a range of liver pathology ranging from simple steatosis to varying degrees of inflammation, hepatocyte injury and fibrosis. Without intervention it can progress to end-stage liver disease and hepatocellular carcinoma. Given its close association with obesity, the prevalence of NAFLD has increased dramatically worldwide. Currently, there are no FDA-approved medications for the treatment of NAFLD and although lifestyle modifications with appropriate diet and exercise have been shown to be beneficial, this has been difficult to achieve and sustain for the majority of patients. As such, the search for effective therapeutic agents is an active area of research. Peroxisome proliferator-activated receptors (PPARs) belong to a class of nuclear receptors. Because of their key role in the transcriptional regulation of mediators of glucose and lipid metabolism, PPAR ligands have been investigated as possible therapeutic agents. Here we review the current evidence from preclinical and clinical studies investigating the therapeutic potential of PPAR ligands for the treatment of NAFLD. •Nonalcoholic fatty liver disease is the most common cause of liver disease.•Without intervention NAFLD can progress to end-stage liver disease.•No therapeutic agents are available for the treatment of NASH.•Peroxisome proliferator-activated receptors regulate lipid and glucose metabolism.•We discuss studies evaluating the efficacy of PPAR agonists for treatment of NASH.
ISSN:0300-9084
1638-6183
DOI:10.1016/j.biochi.2016.11.009