{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T04:28:36Z","timestamp":1792988916471,"version":"4.5.0"},"reference-count":127,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,1,23]]},"abstract":"<jats:p>\n                    Peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3) belongs to a family of nuclear receptors that could serve as lipid sensors. PPAR\u03b3 is the target of a group of insulin sensitizers called thiazolidinediones (TZDs) which regulate the expression of genes involved in glucose and lipid metabolism as well as adipokines that regulate metabolic function in other tissues. Non-alcoholic fatty liver disease (NAFLD) has a high prevalence worldwide and is even higher in patients with obesity and insulin resistance. TZD-mediated activation of PPAR\u03b3 could serve as a good treatment for NAFLD because TZDs have shown anti-fibrogenic and anti-inflammatory effects\n                    <jats:italic>in vitro<\/jats:italic>\n                    and increase insulin sensitivity in peripheral tissues which improves liver pathology. However, mechanistic studies in mouse models suggest that the activation of PPAR\u03b3 in hepatocytes might reduce or limit the therapeutic potential of TZD against NAFLD. In this review, we briefly describe the short history of PPAR isoforms, the relevance of their expression in different tissues, as well as the pathogenesis and potential therapeutics for NAFLD. We also discuss some evidence derived from mouse models that could be useful for endocrinologists to assess tissue-specific roles of PPARs, complement reverse endocrinology approaches, and understand the direct role that PPAR\u03b3 has in hepatocytes and non-parenchymal cells.\n                  <\/jats:p>","DOI":"10.1530\/joe-22-0155","type":"journal-article","created":{"date-parts":[[2023,1,23]],"date-time":"2023-01-23T10:13:57Z","timestamp":1674468837000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":44,"title":["Role of hepatic peroxisome proliferator-activated receptor \u03b3 in non-alcoholic fatty liver disease"],"prefix":"10.1530","volume":"257","author":[{"given":"Samuel M","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose","family":"Muratalla","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Sierra-Cruz","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8787-2706","authenticated-orcid":true,"given":"Jose","family":"Cordoba-Chacon","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Nature Medicine","first-page":"557","article-title":"PPARgamma signaling and metabolism: the good, the bad and the future","volume":"19","author":"Ahmadian","year":"2013","unstructured":"Ahmadian MSuh JMHah NLiddle CAtkins ARDownes MEvans RM2013PPARgamma signaling and metabolism: the good, the bad and the future. 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