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Does prenylation predict progression in NAFLD?

Peyman Ghorbani1,2, Tyler Kt Smith1,2, Morgan D Fullerton1,2,3

  • 1Centre for Infection, Immunity and Inflammation, Ottawa, Ontario, Canada.

The Journal of Pathology
|October 31, 2018
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Summary
This summary is machine-generated.

Metabolites of the mevalonate pathway, specifically geranylgeranyl diphosphate synthase (GGPPS), may regulate the progression of non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH). GGPPS dysregulation impairs lipid oxidation despite increased AMPK activation in NASH.

Keywords:
GGPPSMx1-CreNAFLDNASHRab7diabetesfatty liverfibrosisgeranylgeranylationmetabolic syndromemevalonate pathwaymitophagyobesityprotein prenylation

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Area of Science:

  • Hepatology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Non-alcoholic fatty liver disease (NAFLD) is linked to metabolic conditions like obesity and insulin resistance.
  • Progression from NAFLD to non-alcoholic steatohepatitis (NASH) is driven by lipid accumulation and inflammation.
  • Triggers for NAFLD progression to NASH remain poorly understood.

Purpose of the Study:

  • Investigate the role of mevalonate pathway metabolites in NASH progression.
  • Examine the function of geranylgeranyl diphosphate synthase (GGPPS) in NASH.
  • Understand the impact of GGPPS dysregulation on lipid metabolism and mitochondrial function.

Main Methods:

  • Studied GGPPS dysregulation in human and mouse models of NASH.
  • Analyzed the effects of GGPPS deletion/knockdown on protein prenylation (farnesylation and geranylgeranylation).
  • Assessed liver lipid oxidation and mitochondrial function in Ggpps-deficient mice on a high-fat diet.

Main Results:

  • GGPPS is dysregulated in NASH.
  • GGPPS deficiency promotes farnesylation and augments liver kinase B1/AMPK signaling.
  • Ggpps-deficient mice exhibit impaired lipid oxidation and mitochondrial dysfunction despite increased AMPK activation.

Conclusions:

  • The mevalonate pathway, particularly GGPPS, plays a role in regulating NASH progression.
  • Dysregulation of GGPPS impacts lipid metabolism and mitochondrial function in NASH.
  • Further research is needed to explore the therapeutic and diagnostic potential of the mevalonate pathway in NAFLD.