Impaired liver regeneration and lipid homeostasis in CCl treated WDR13 deficient mice.

WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Lepr mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13 mice using hepatotoxin CCl. In the present study we report slower hepatic regeneration in Wdr13 mice as compared to their wild type littermates after CCl administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13 mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl- administered Wdr13 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl administered Wdr13 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.