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Significance The liver plays a central role in systemic metabolism. Hepatocytes rarely proliferate in normal liver, but these cells readily enter the cell cycle after injuries that reduce functional hepatic mass. Prior studies have documented that metabolic functions of the liver are transiently downregulated during liver regeneration, but the underlying mechanisms are poorly understood. Here, we demonstrate that cyclin D1 and HNF4α, the best-characterized intracellular mediators of hepatocyte proliferation and differentiation (respectively), are reciprocal negative regulatory partners that control both cell cycle progression and metabolism in the liver. Repression of HNF4α transcriptional activity by cyclin D1 provides a mechanism by which liver metabolic function is broadly attenuated during regeneration and potentially other contexts.

A negative reciprocal regulatory axis between cyclin D1 and HNF4α modulates cell cycle progression and metabolism in the liver