{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T16:42:39Z","timestamp":1786725759297,"version":"build-2736575974"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background and purpose:<\/jats:title>\n                    <jats:p>Non-alcoholic fatty liver disease (NAFLD) is the most common liver-related metabolic disorder worldwide, affecting approximately 25% of the global population. Peroxisome proliferator-activated receptor (PPAR) agonists play an important role in NAFLD management through modulation of lipid metabolism and insulin sensitivity. This study compared the effects of fenofibrate (PPAR\u03b1 agonist), pioglitazone (PPAR\u03b3 agonist), and saroglitazar (dual PPAR\u03b1\/\u03b3 agonist) in a high-fat diet (HFD)-induced NAFLD rat model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental approach:<\/jats:title>\n                    <jats:p>NAFLD was induced in Wistar rats by feeding a high-fat diet. Animals were assigned to control, HFD, and HFD-treated groups receiving saroglitazar (3 mg\/kg), pioglitazone (30 mg\/kg), or fenofibrate (100 mg\/kg) for six weeks. Anthropometric parameters, serum liver enzymes, lipid profile, fasting blood glucose, and HOMA-IR were assessed. Histopathological changes were evaluated using H&amp;E and Masson\u2019s trichrome staining. Hepatic expression of FGF21, CPT-1, PPARa, SREBP-1c, and ACC was analyzed by quantitative RT-PCR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings\/Results:<\/jats:title>\n                    <jats:p>All three PPAR agonists significantly improved hepatic steatosis, inflammation, and fibrosis compared with the HFD group, despite variability in biochemical and metabolic parameters. Among the treatments, saroglitazar demonstrated the most pronounced histological improvement, although systemic metabolic improvements were comparable among all three agents.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and implications:<\/jats:title>\n                    <jats:p>Fenofibrate, pioglitazone, and saroglitazar exert beneficial effects on NAFLD progression through partially distinct mechanisms. Dual PPAR\u03b1\/\u03b3 activation appears to preferentially enhance hepatic histological outcomes, supporting the therapeutic relevance of saroglitazar in NAFLD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/rps.rps_182_25","type":"journal-article","created":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T06:00:56Z","timestamp":1778479256000},"page":"292-304","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Effects of PPAR\u03b1, PPAR\u03b3, and dual PPAR\u03b1\/\u03b3 agonists on liver tissue and biochemical markers in NAFLD-induced Wistar rats"],"prefix":"10.4103","volume":"21","author":[{"given":"Elham","family":"Khoshbakht","sequence":"first","affiliation":[{"name":"Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Negar","family":"Dinarvand","sequence":"additional","affiliation":[{"name":"Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamid","family":"Yaghooti","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Behrouz","family":"Taheri","sequence":"additional","affiliation":[{"name":"Department of Medical Biotechnology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Narges","family":"Mohammadtaghvaei","sequence":"additional","affiliation":[{"name":"Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, 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