ArticleScientific reports2022
Therapeutic effects of isosteviol sodium on non-alcoholic fatty liver disease by regulating autophagy via Sirt1/AMPK pathway.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- The alteration of brain function in overweight/obese individuals and the neurological benefit of thymoquinone: uncovering molecular mechanisms.Metabolic brain disease · 2026Review
- Induction of Autophagy as a Therapeutic Breakthrough for NAFLD: Current Evidence and Perspectives.Biology · 2025Review
- Article
- Structure, Properties, and Biomedical Activity of Natural Sweeteners Steviosides: An Update.Food science & nutrition · 2025Review
- Review
- Potential Synergistic Effects of Caffeine and Naringin on Mitochondrial Biogenesis and Hepatic Steatosis in Adult Male Rats With NAFLD Induced by a High-Fat Diet.BioMed research international · 2025Article
- Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease.Biomolecules · 2024Review
- Circ_0004535/miR-1827/CASP8 network involved in type 2 diabetes mellitus with nonalcoholic fatty liver disease.Scientific reports · 2023Article
- Red Pepper Seeds Inhibit Hepatic Lipid Accumulation by Inducing Autophagy via AMPK Activation.Nutrients · 2022Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isosteviol sodium (STVNa) is a beyerane diterpene synthesized via acid hydrolysis of stevioside, which can improve glucose and lipid metabolism in animals with diabetes. However, it remains unknown whether STVNa can exhibit a therapeutic effect on nonalcoholic fatty liver disease (NAFLD) and its underlying mechanism. We hypothesize that autophagic initiation may play a key role in mediating the development of NAFLD. Herein, we assessed the effects of STVNa on NAFLD and its underlying mechanisms. The results demonstrated that STVNa treatment effectively ameliorated NAFLD in rats fed high-fat diet (HFD). Moreover, STVNa decreased the expression of inflammation-related genes and maintained a balance of pro-inflammatory cytokines in NAFLD rats. STVNa also reduced lipid accumulation in free fatty acid (FFA)-exposed LO2 cells. In addition, STVNa attenuated hepatic oxidative stress and fibrosis in NAFLD rats. Furthermore, STVNa enhanced autophagy and activated Sirtuin 1/adenosine monophosphate-activated protein kinase (Sirt1/AMPK) pathway both in vivo and in vitro, thus attenuating intracellular lipid accumulation. In summary, STVNa could improve lipid metabolism in NAFLD by initiating autophagy via Sirt1/AMPK pathway. Therefore, STVNa may be an alternative therapeutic agent for treatment of NAFLD.
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