Impaired liver regeneration and lipid homeostasis in CCl(4) 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(db/db) 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(−/0) mice using hepatotoxin CCl(4). In the present study we report slower hepatic regeneration in Wdr13(−/0) mice as compared to their wild type littermates after CCl(4) administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13(−/0) mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl(4)- administered Wdr13(−/0) mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl(4) administered Wdr13(−/0) mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s42826-020-00076-8.