ArticleMolecular medicine reports2019
Hydrogen sulfide protects against high glucose‑induced lipid metabolic disturbances in 3T3‑L1 adipocytes via the AMPK signaling pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- The therapeutic potential of hydrogen sulfide and its donors, a new discovery in vascular diseases.Journal of cardiovascular pharmacology · 2025Article
- The Janus Face of Oxidative Stress and Hydrogen Sulfide: Insights into Neurodegenerative Disease Pathogenesis.Antioxidants (Basel, Switzerland) · 2025Review
- Ageing-Related Alterations in Renal Epithelial Glucose Transport.International journal of molecular sciences · 2023Article
- Vasoactive Effects of Chronic Treatment with Fructose and Slow-Releasing HInternational journal of molecular sciences · 2022Article
- Chronic and Transient Hyperglycemia Induces Changes in the Expression Patterns ofInternational journal of molecular sciences · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Aberrant lipid metabolism contributes to the development of type 2 diabetes mellitus. The mechanisms by which hydrogen sulfide (H2S), an endogenous gasotransmitter, regulates lipid metabolism remain unclear. The aim of the present study was to investigate if the protective effects of H2S during high glucose (HG)‑induced lipid accumulation in 3T3‑L1 adipocytes may be mediated by AMP‑activated protein kinase (AMPK). Triglyceride (TG) content and the production of H2S were determined using adipogenesis colorimetric assay kits and H2S synthesis methods. The levels of monocyte chemoattractant protein‑1 and adiponectin were evaluated by ELISA. Total AMPK and phosphorylated AMPK levels were assessed by western blot analysis. HG increased the cellular level of TG and decreased H2S production in 3T3‑L1 adipocytes. The H2S donor, sodium hydrosulfide (NaHS) protected against the HG‑induced accumulation of TG in 3T3‑L1 adipocytes. Furthermore, NaHS suppressed HG‑induced TG accumulation by activating AMPK. Collectively, the findings of the present study suggested that HG induced lipid accumulation in 3T3‑L1 adipocytes, and AMPK activation may underlie the lipid‑lowering effects of H2S.
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