No obvious pathological symptoms such as inflammation were observed in fatty goose liver, suggesting that there is a unique mechanism to inhibit the development of inflammation during the goose fatty liver formation. Previous studies have shown that high glucose activated the ubiquitin–proteasome. Protein kinase A (PKA) can interact with a key protein in the nuclear factor-kappaB pathway to activate the pathway and trigger inflammatory response. To further understand how inflammation is suppressed during goose fatty liver formation. The present study showed that inflammation and PKA protein level were reduced in goose fatty liver. Meanwhile, PKA can be modified by ubiquitination in goose liver and hepatocytes. The result of the study implied that glucose deposited during goose fatty liver formation may reduce the PKA protein content by increasing the PKA ubiquitination level, thereby inhibiting the inflammatory response. Our study not only contributes to elucidate the new mechanism for suppressed inflammation in goose fatty liver but also provides a reference for the study of fatty liver in other animals.

Read the full article in the Journal of Animal Science.