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PPAR Research
Volume 2016, Article ID 7403230, 18 pages
Review Article

PPARs and Mitochondrial Metabolism: From NAFLD to HCC

1Clinical Gastroenterology Unit, Department of Biomedical Clinical and Experimental Sciences “Mario Serio”, University of Florence, Viale Pieraccini 6, 50129 Florence, Italy
2Careggi University Hospital, Florence, Italy

Received 22 July 2016; Revised 8 November 2016; Accepted 10 November 2016

Academic Editor: Daniele Fanale

Copyright © 2016 Tommaso Mello et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Metabolic related diseases, such as type 2 diabetes, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD), are widespread threats which bring about a significant burden of deaths worldwide, mainly due to cardiovascular events and cancer. The pathogenesis of these diseases is extremely complex, multifactorial, and only partially understood. As the main metabolic organ, the liver is central to maintain whole body energetic homeostasis. At the cellular level, mitochondria are the metabolic hub connecting and integrating all the main biochemical, hormonal, and inflammatory signaling pathways to fulfill the energetic and biosynthetic demand of the cell. In the liver, mitochondria metabolism needs to cope with the energetic regulation of the whole body. The nuclear receptors PPARs orchestrate lipid and glucose metabolism and are involved in a variety of diseases, from metabolic disorders to cancer. In this review, focus is placed on the roles of PPARs in the regulation of liver mitochondrial metabolism in physiology and pathology, from NAFLD to HCC.