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HLF and PPARα axis regulates metabolic-associated fatty liver disease through extracellular vesicles derived from the

Xingzhen Yang1, Jiale Wang1, Xinyu Qi1

  • 1Guangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology Guangxi University Nanning China.

Imeta
|April 16, 2025
PubMed

Insights

Hepatic leukemia factor (HLF) in the intestine alleviates metabolic-associated fatty liver disease (MAFLD) by regulating lipid absorption and gut microbiota. This pathway involves extracellular vesicles and taurochenodeoxycholic acid, offering a new therapeutic target for MAFLD.

Area of Science:

  • Gastroenterology and Hepatology
  • Molecular Biology
  • Metabolic Disorders

Background:

  • Metabolic-associated fatty liver disease (MAFLD) prevalence is rising globally.
  • The intestine plays a crucial role in lipid metabolism and homeostasis.
  • Mechanisms linking intestinal function to MAFLD pathogenesis require further elucidation.

Purpose of the Study:

  • To investigate the role of hepatic leukemia factor (HLF) in intestinal lipid absorption and MAFLD development.
  • To identify the molecular pathways and mediators involved in HLF's effect on MAFLD.

Main Methods:

  • Single-cell transcriptome analysis of intestinal tissue from cynomolgus monkeys.
  • Intestine-specific Hlf-knockout mouse models.
  • Lipidomics and functional experiments.

Main Results:

  • HLF regulates intestinal lipid absorption and alleviates intestinal barrier dysfunction by inhibiting PPARα expression.
  • The HLF/PPARα axis modulates gut microbiota-derived extracellular vesicles (fEVs).
  • fEVs containing taurochenodeoxycholic acid (TCDCA) inhibit hepatocyte ferroptosis, ameliorating MAFLD.

Conclusions:

  • Intestinal HLF activity, mediated by fEVs and TCDCA, is a novel mechanism in MAFLD pathogenesis.
  • HLF represents a potential therapeutic target for managing MAFLD.
Keywords:
HLFMAFLDbile acidsextracellular vesiclesferroptosisgut microbiome

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