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 Leprdb/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 CCl4. In the present study we report slower hepatic regeneration in Wdr13−/0 mice as compared to their wild type littermates after CCl4 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 CCl4- administered Wdr13 −/0 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl4 administered Wdr13 −/0 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.

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 Leprdb/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 CCl4. In the present study we report slower hepatic regeneration in Wdr13−/0 mice as compared to their wild type littermates after CCl4 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 CCl4- administered Wdr13 −/0 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl4 administered Wdr13 −/0 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.