{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T21:46:48Z","timestamp":1792705608963,"version":"4.5.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2021,7,19]],"date-time":"2021-07-19T00:00:00Z","timestamp":1626652800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2021,7,19]],"date-time":"2021-07-19T00:00:00Z","timestamp":1626652800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2021,10]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>NAFLD is characterized by insulin resistance and dysregulated lipid and glucose metabolism. Saroglitazar, a dual peroxisome proliferator activated receptor\u2010\u03b1\/\u03b3 agonist, improves insulin sensitivity, and lipid and glycemic parameters. Saroglitazar improved NASH histology in animal studies. In this randomized controlled clinical trial, we evaluated the efficacy and safety of saroglitazar in patients with NAFLD\/NASH.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results<\/jats:title>\n                    <jats:p>\n                      A total of 106 patients with NAFLD\/NASH with alanine aminotransferase (ALT)\u00a0\u2265\u00a050\u00a0U\/L at baseline and body mass index \u226525\u00a0kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      were randomized in a 1:1:1:1 ratio to receive placebo or saroglitazar 1\u00a0mg, 2\u00a0mg, or 4\u00a0mg for 16\u00a0weeks. The primary efficacy endpoint was percentage change from baseline in ALT levels at week 16. Liver fat content (LFC) was assessed by MRI proton density fat fraction. The least\u2010squares mean percent change from baseline in ALT at week 16 was \u221225.5% (5.8), \u221227.7% (5.9), and \u221245.8% (5.7), with saroglitazar 1\u00a0mg, 2\u00a0mg, and 4\u00a0mg, respectively, versus 3.4% (5.6) in placebo (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u00a0&lt;\u00a00.001 for all). Compared with placebo, saroglitazar 4\u00a0mg improved LFC (4.1% [5.9] vs. \u221219.7% [5.6]), adiponectin (\u22120.3\u00a0\u03bcg\/mL [0.3] vs. 1.3\u00a0\u03bcg\/mL [0.3]), homeostatic model assessment\u2013insulin resistance (\u22121.3 [1.8] vs. \u22126.3 [1.7]), and triglycerides (\u22125.3\u00a0mg\/dL [10.7] vs. \u221268.7\u00a0mg\/dL [10.3]) (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u00a0&lt;\u00a00.05 for all). Saroglitazar 4\u00a0mg also improved lipoprotein particle composition and size and reduced lipotoxic lipid species. Saroglitazar was well\u2010tolerated. A mean weight gain of 1.5\u00a0kg was observed with saroglitazar 4\u00a0mg versus 0.3\u00a0kg with placebo (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u00a0=\u00a00.27).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Saroglitazar 4\u00a0mg significantly improved ALT, LFC, insulin resistance, and atherogenic dyslipidemia in participants with NAFLD\/NASH. (ClinicalTrials.gov identifier: NCT03061721.)<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.31843","type":"journal-article","created":{"date-parts":[[2021,4,3]],"date-time":"2021-04-03T01:07:08Z","timestamp":1617412028000},"page":"1809-1824","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":367,"title":["Saroglitazar, a PPAR\u2010\u03b1\/\u03b3 Agonist, for Treatment of NAFLD: A Randomized Controlled Double\u2010Blind Phase 2 Trial"],"prefix":"10.1097","volume":"74","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2056-4909","authenticated-orcid":false,"given":"Samer","family":"Gawrieh","sequence":"first","affiliation":[{"name":"Gastroenterology & Hepatology,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mazen","family":"Noureddin","sequence":"additional","affiliation":[{"name":"Digestive and Liver Diseases,Cedars Sinai Medical 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V.","family":"Kowdley","sequence":"additional","affiliation":[{"name":"Liver Institute Northwest,Seattle,WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle","family":"Lai","sequence":"additional","affiliation":[{"name":"Gastroenterology and Hepatology,Beth Israel Deaconess Medical Center,Boston,MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugene","family":"Schiff","sequence":"additional","affiliation":[{"name":"Schiff Center for Liver Diseases,University of Miami School of Medicine,Miami,FL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deven","family":"Parmar","sequence":"additional","affiliation":[{"name":"Zydus Discovery DMCC,Dubai,UAE"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pankaj","family":"Patel","sequence":"additional","affiliation":[{"name":"Zydus Research Centre,Cadila Healthcare 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