title: Hydrogen sulfide improves glucose metabolism and prevents hypertrophy in cardiomyocytes.
abstract: BACKGROUND
  Hydrogen sulfide (H2S) has been reported to inhibit myocardial hypertrophy in a cell model of cardiomyocyte hypertrophy. Our previous study also shows an H2S-induced increase in glucose metabolism in insulin-targeting cells. The present study aims to examine the hypothesis that H2S attenuates myocardial hypertrophy and promotes glucose utilization in cardiomyocytes.
  
  
  METHODS
  The cell model of cardiomyocyte hypertrophy was induced by application of phenylephrine and cardiomyocyte hypertrophy was examined using leucine incorporation assay. Protein levels were measured using Western blot analysis. The activity of related enzymes was measured with enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  NaHS (an H2S donor) treatment increased the activity of cultured cardiomyocytes and reduced hypertrophy in cultured cardiomyocytes at concentrations ranging from 25 to 200 µmol/L. NaHS treatment increased glucose uptake and the efficiency of glycolysis and the citric acid cycle. The key enzymes in these reactions, including lactate dehydrogenase and pyruvate kinase and succinate dehydrogenase, were activated by NaHS treatment (100 µmol/L). Some intermediates of glycolysis and the citric acid cycle, including lactic acid, cyclohexylammonium, oxaloacetic acid, succinate, L-dimalate, sodium citrate, cis-aconitic acid, ketoglutarate and DL-isocitric acid trisodium also showed anti-hypertrophic effects in cardiomyocytes.
  
  
  CONCLUSIONS
  H2S improves glucose utilization and inhibits cardiomyocyte hypertrophy.
authors.affiliation: Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai Medical College, Shanghai, China.
authors.forename: Min
authors.initials: M
authors.lastname: Liang
authors.affiliation: Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai Medical College, Shanghai, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Jin
authors.affiliation: Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai Medical College, Shanghai, China.
authors.forename: Dong-Dong
authors.initials: DD
authors.lastname: Wu
authors.affiliation: Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai Medical College, Shanghai, China.
authors.forename: Ming-Jie
authors.initials: MJ
authors.lastname: Wang
authors.affiliation: Shanghai Key Laboratory of Bioactive Small Molecules and Research Center on Aging and Medicine, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University Shanghai Medical College, Shanghai, China. Electronic address: yczhu@shmu.edu.cn.
authors.forename: Yi-Chun
authors.initials: YC
authors.lastname: Zhu
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D049108:Cell Enlargement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002952:Citric Acid Cycle / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D006352:Heart Ventricles / Q000166:cytology; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010656:Phenylephrine; D051381:Rats
chemical_list: D010656:Phenylephrine; D000255:Adenosine Triphosphate; D005947:Glucose; D006862:Hydrogen Sulfide
keywords: Cardiac hypertrophy; Glucose transporter; Hydrogen sulfide