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Brain-derived neurotrophic factor knock-out mice develop non-alcoholic steatohepatitis.

Mayuko Ichimura-Shimizu1, Masami Kojima2,3,4, Shingo Suzuki5,6

  • 1Department of Pathology and Laboratory Medicine, Tokushima University Graduate School, Tokushima, Japan.

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|October 2, 2023
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Summary

Reduced brain-derived neurotrophic factor (BDNF) expression is linked to weight gain and non-alcoholic steatohepatitis (NASH) in mice. This study reveals BDNF

Keywords:
RNA sequencingbrain-derived neurotrophic factorgene ontologyliver fibrosismouse modelnon-alcoholic fatty liver diseasenon-alcoholic steatohepatitis

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Area of Science:

  • Metabolic disease research
  • Neuroscience
  • Hepatology

Background:

  • Brain-derived neurotrophic factor (BDNF) is known to regulate food intake and body weight.
  • The role of BDNF in peripheral diseases, such as chronic liver conditions, remains unclear.
  • Non-alcoholic steatohepatitis (NASH) is a severe form of non-alcoholic fatty liver disease, a hepatic manifestation of metabolic syndrome.

Purpose of the Study:

  • To investigate the role of reduced brain-derived neurotrophic factor (BDNF) expression in the pathogenesis of non-alcoholic steatohepatitis (NASH).
  • To explore the association between BDNF levels, obesity, and liver pathology in a mouse model.

Main Methods:

  • Utilized BDNF-heterozygous (BDNF+/-) and knock-in (BDNF+/pro) mice to model reduced BDNF expression.
  • Conducted histopathological analysis of liver and visceral fat tissues.
  • Performed RNA sequencing (RNA-seq) on liver tissue to analyze gene expression patterns.
  • Implemented a food restriction study in pair-fed BDNF+/pro mice.

Main Results:

  • BDNF+/- mice exhibited key NASH features, including steatosis, inflammation, hepatocyte ballooning, fibrosis, obesity, and elevated glucose and insulin levels.
  • RNA-seq identified enriched pathways related to fatty acid metabolism and neutrophil aggregation in the liver, alongside indicators of oxidative stress.
  • Pair-fed BDNF+/pro mice developed liver damage and inflammation, irrespective of body weight, indicating a direct role of reduced BDNF in liver pathology.

Conclusions:

  • Reduced BDNF expression is a significant factor in the development of non-alcoholic steatohepatitis (NASH).
  • This study provides the first evidence linking decreased BDNF to the pathogenic mechanisms underlying NASH.
  • BDNF deficiency contributes to liver disease independently of obesity through mechanisms involving inflammation and metabolic dysregulation.