Serum amyloid A1 exacerbates hepatic steatosis via TLR4-mediated NF-κB signaling pathway.

ABSTRACT:

Objective

Chronic inflammatory response plays a prominent role in obesity-related nonalcoholic fatty liver disease (NAFLD). However, the intrahepatic triggering mechanism of inflammation remains obscure. This study aimed to elucidate the role of serum amyloid A1 (SAA1), an acute-phase response protein, in the obesity-induced hepatic inflammation and NAFLD.

Methods

Male mice were fed a high fat diet (HFD) for 16 weeks, and insulin resistance, hepatic steatosis, and inflammation in mice were monitored. Murine SAA1/2 was genetically manipulated to investigate the role of SAA1 in NAFLD.

Results

We found that SAA1 was increased in the NAFLD liver in both humans and mice. Knockout of SAA1/2 or knockdown of hepatic SAA1/2 promoted energy expenditure and alleviated HFD-induce

SUBMITTER: Jiang B 

PROVIDER: S-EPMC8938331 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature