PRIMA1 participates in the inhibition of inflammation and acetylcholinesterase activity in goose fatty liver formation.

Abstract

Goose fatty liver, a product of short-term overfeeding, is notable for its high nutritional value and unique tolerance to severe steatosis without inflammation, in contrast to human nonalcoholic fatty liver disease (NAFLD). It is known that choline can alleviate nonalcoholic steatohepatitis and liver cirrhosis, inhibit cell apoptosis, promote lecithin synthesis and fat transportation out of the liver, and relieve cardiovascular disease-related symptoms (e.g., hyperlipidemia and hypercholesterolemia). This study investigates the role of Proline Rich Membrane Anchor 1 (PRIMA1) in inhibiting inflammation through choline metabolism during goose fatty liver formation. Overfeeding of geese resulted in increased body and liver weights, elevated fat content, and significantly higher expression of PRIMA1, accompanied by decreased LITAF and CRP (important pro-inflammatory cytokines) expression and reduced acetylcholinesterase (AchE) activity, which was assessed by the amount of produced choline. The overexpression of PRIMA1 in goose primary hepatocytes (GPHs) enhanced AchE activity. Consistently, glucose-induced upregulation of PRIMA1 expression in GPHs was accompanied by increased AchE activity. Further combined treatment with glucose and PRIMA1 knockdown in GPHs showed that downregulation of PRIMA1 attenuated the suppression of LITAF and CRP expression caused by glucose addition, but had no effect on the rise in AchE activity. These findings indicate that PRIMA1 may play a role in promoting choline metabolism and protecting against liver inflammation, offering insights into potential therapeutic targets for NAFLD.