Impaired liver regeneration and lipid homeostasis in CCl4 treated WDR13 deficient mice
10.1186/s42826-020-00076-8
- Author:
Arun Prakash MISHRA
1
;
Archana B. SIVA
;
Chandrashekaran GURUNATHAN
;
Y. KOMALA
;
B. Jyothi LAKSHMI
Author Information
1. CSIR- Centre for Cellular and Molecular Biology, Hyderabad 500007, India
- Publication Type:Research
- From:Laboratory Animal Research
2020;36(4):318-327
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
