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Cyclin D1 inhibits hepatic lipogenesis via repression of carbohydrate response element binding protein and hepatocyte

Eric A Hanse1, Douglas G Mashek, Jennifer R Becker

  • 1Division of Gastroenterology, Hennepin County Medical Center, Minneapolis, MN, USA.

Cell Cycle (Georgetown, Tex.)
|July 4, 2012
PubMed

Insights

Cyclin D1 impairs liver lipogenesis by repressing key transcription factors, linking cell cycle control to metabolic regulation during liver regeneration and injury.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Liver metabolic capacity is altered post-injury during compensatory hepatocyte proliferation.
  • Mechanisms linking cell cycle progression to metabolic changes remain unclear.

Purpose of the Study:

  • To investigate the role of cyclin D1 in regulating de novo lipogenesis.
  • To elucidate the molecular mechanisms by which cyclin D1 influences lipogenic gene expression.

Main Methods:

  • Primary hepatocyte culture and gene expression analysis.
  • Study of transcription factors carbohydrate response element-binding protein (ChREBP) and hepatocyte nuclear factor 4α (HNF4α).
  • In vivo studies in mouse liver during carbohydrate feeding and regeneration.

Main Results:

  • Cyclin D1 significantly impaired glucose-stimulated lipogenesis and inhibited key lipogenic genes.
  • Cyclin D1 repressed both ChREBP and HNF4α activity, affecting their transcriptional functions.
  • Cyclin D1 inhibited HNF4α recruitment to lipogenic gene promoters via Cdk4-dependent and -independent pathways.

Conclusions:

  • Cyclin D1 acts as a repressor of ChREBP and HNF4α in hepatocytes.
  • These findings establish a direct link between the cell cycle machinery and metabolic control in the liver.

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