ArticleScientific reports2020
The PPAR α/γ Agonist Saroglitazar Improves Insulin Resistance and Steatohepatitis in a Diet Induced Animal Model of Nonalcoholic Fatty Liver Disease.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 107 citations in OpenAlex.
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- Recent advances in the design, development and therapeutic applications of PPARγ agonists.Future medicinal chemistry · 2025Review
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- Identification of diagnostic hub genes related to energy metabolism in idiopathic pulmonary fibrosis.Frontiers in molecular biosciences · 2025Article
- Novel role of Quercetin in ameliorating metabolic syndrome via VDR mediated activation of adiponectin/AdipoR2 signaling.Biochemistry and biophysics reports · 2024Article
- Application of PPAR Ligands and Nanoparticle Technology in Metabolic Steatohepatitis Treatment.Biomedicines · 2024Review
- Altered Mitochondrial Function in MASLD: Key Features and Promising Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2024Review
- New advances in drug development for metabolic dysfunction-associated diseases and alcohol-associated liver disease.Cell & bioscience · 2024Review
- The role of lipid metabolism in osteoporosis: Clinical implication and cellular mechanism.Genes & diseases · 2024Review
- Intervention effect of Cigu Xiaozhi prescription on ceramide lipoapoptosis in non-alcoholic fatty liver disease.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- New Therapeutic Approaches for the Treatment of Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Increased Cardiovascular Risk.Diagnostics (Basel, Switzerland) · 2024Review
- Research Progress of Natural Products with the Activity of Anti-nonalcoholic Steatohepatitis.Mini reviews in medicinal chemistry · 2024Review
- The Role of Nuclear Receptors in the Pathogenesis and Treatment of Non-alcoholic Fatty Liver Disease.International journal of biological sciences · 2024Review
- Molecular mechanisms of alcohol's effects on the human body: A review and update.Journal of biochemical and molecular toxicology · 2023Review
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- Pharmaceutical Strategies to Improve Druggability of Potential Drug Candidates in Nonalcoholic Fatty Liver Disease Therapy.Pharmaceutics · 2023Review
- Antioxidant Peptides from Monkfish Swim Bladders: Ameliorating NAFLD In Vitro by Suppressing Lipid Accumulation and Oxidative Stress via Regulating AMPK/Nrf2 Pathway.Marine drugs · 2023Article
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance and hepatic lipid accumulation constitute the metabolic underpinning of nonalcoholic steatohepatitis (NASH). We tested the hypothesis that saroglitazar, a PPAR α/γ agonist would improve NASH in the diet-induced animal model of NAFLD. Mice received chow diet and normal water (CDNW) or high fat western diet and ad lib sugar water (WDSW). After 12 weeks, WDSW fed mice were randomized to receive (1) WDSW alone, (2) WDSW + vehicle, (3) WDSW + pioglitazone or (4) WDSW + saroglitazar for an additional 12 weeks. Compared to mice on WDSW and vehicle controls, mice receiving WDSW + saroglitazar had lower weight, lower HOMA-IR, triglycerides, total cholesterol, and ALT. Saroglitazar improved steatosis, lobular inflammation, hepatocellular ballooning and fibrosis stage. NASH resolved in all mice receiving saroglitazar. These effects were at par with or superior to pioglitazone. Molecular analyses confirmed target engagement and reduced oxidative stress, unfolded protein response and fibrogenic signaling. Transcriptomic analysis further confirmed increased PPAR-target expression and an anti-inflammatory effect with saroglitazar. Lipidomic analyses demonstrated that saroglitazar also reduced triglycerides, diglycerides, sphingomyelins and ceramides. These preclinical data provide a strong rationale for developing saroglitazar for the treatment of NASH in humans.
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