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Vitamin B12 and folate decrease inflammation and fibrosis in NASH by preventing syntaxin 17 homocysteinylation.

Madhulika Tripathi1, Brijesh Kumar Singh1, Jin Zhou1

  • 1Laboratory of Hormonal Regulation, Cardiovascular and Metabolic Disorders, Duke-NUS Medical School, Singapore 169857.

Journal of Hepatology
|July 12, 2022
PubMed
Summary
This summary is machine-generated.

Hyperhomocysteinemia (HHcy) drives non-alcoholic steatohepatitis (NASH) by affecting protein stability and autophagy. Supplementation with vitamin B12 and folate can reverse NASH progression and offers a potential therapeutic strategy.

Keywords:
AutophagyB(12)FibrosisFolateHomocysteineNon-alcoholic steatohepatitis (NASH)Protein homocysteinylationSyntaxin-17Vitamin therapy

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Area of Science:

  • Hepatology and Metabolic Diseases
  • Molecular Biology and Biochemistry
  • Nutritional Science

Background:

  • Non-alcoholic steatohepatitis (NASH) is a growing health concern with limited therapeutic options.
  • Clinical studies suggest correlations between serum homocysteine (Hcy) and NASH severity, but HHcy's pathogenic role remains unclear.

Purpose of the Study:

  • To investigate the pathogenic role of hyperhomocysteinemia (HHcy) in non-alcoholic steatohepatitis (NASH) progression.
  • To explore the potential of vitamin B12 (B12) and folate (Fol) as therapeutic agents for NASH.

Main Methods:

  • Examined HHcy effects on NASH in mouse models, primates, and human patients.
  • Utilized vitamin B12 and folate supplementation to reverse NASH features in vitro and in vivo.
  • Analyzed protein homocysteinylation, ubiquitination, autophagy markers, and hepatic histology.

Main Results:

  • Elevated hepatic Hcy levels induced and worsened NASH, correlating with inflammation and fibrosis.
  • HHcy led to homocysteinylation and ubiquitination of hepatic proteins, including Syntaxin 17 (Stx17), impairing autophagy.
  • Vitamin B12/folate supplementation reduced HHcy, restored Stx17 and autophagy, improved fatty acid metabolism, and ameliorated liver histology in established NASH.

Conclusions:

  • HHcy plays a critical role in NASH pathogenesis through Stx17 homocysteinylation and subsequent autophagy dysfunction.
  • Vitamin B12 and folate supplementation demonstrate significant therapeutic potential for NASH treatment and prevention.