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Background & Aims  Non‐alcoholic fatty liver disease ( NAFLD ) and non‐alcoholic steatohepatitis ( NASH ) are common clinico‐pathological conditions that affect millions of patients worldwide. In this study, the efficacy of saroglitazar, a novel  PPAR α/γ agonist, was assessed in models of  NAFLD / NASH .    Methods & Results  HepG2 cells treated with palmitic acid ( PA ;0.75  mM ) showed decreased expression of various antioxidant biomarkers ( SOD 1,  SOD 2, glutathione peroxidase and catalase) and increased expression of inflammatory markers ( TNF α,  IL 1β and  IL 6). These effects were blocked by saroglitazar, pioglitazone and fenofibrate (all tested at 10μM concentration). Furthermore, these agents reversed  PA ‐mediated changes in mitochondrial dysfunction,  ATP  production,  NF kB phosphorylation and stellate cell activation in HepG2 and HepG2‐ LX 2 Coculture studies. In mice with choline‐deficient high‐fat diet‐induced  NASH , saroglitazar reduced hepatic steatosis, inflammation, ballooning and prevented development of fibrosis. It also reduced serum alanine aminotransferase, aspartate aminotransferase and expression of inflammatory and fibrosis biomarkers. In this model, the reduction in the overall  NAFLD  activity score by saroglitazar (3 mg/kg) was significantly more prominent than pioglitazone (25 mg/kg) and fenofibrate (100 mg/kg). Pioglitazone and fenofibrate did not show any improvement in steatosis, but partially improved inflammation and liver function. Antifibrotic effect of saroglitazar (4 mg/kg) was also observed in carbon tetrachloride‐induced fibrosis model.    Conclusions  Saroglitazar, a dual  PPAR α/γ agonist with predominant  PPAR α activity, shows an overall improvement in  NASH . The effects of saroglitazar appear better than pure  PPAR α agonist, fenofibrate and  PPAR γ agonist pioglitazone.

Dual PPAR α/γ agonist saroglitazar improves liver histopathology and biochemistry in experimental NASH models