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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.

Impaired liver regeneration and lipid homeostasis in CCl4 treated WDR13 deficient mice