PKCε contributes to chronic ethanol-induced steatosis in mice but not inflammation and necrosis.

ABSTRACT:

Background

Protein kinase C epsilon (PKCε) has been shown to play a role in experimental steatosis by acute alcohol. The "two-hit" hypothesis implies that preventing steatosis should blunt more advanced liver damage (e.g., inflammation and necrosis). However, the role of PKCε in these pathologies is not yet known. The goal of this current work was to address this question in a model of chronic alcohol exposure using antisense oligonucleotides (ASO) against PKCε.

Methods

Accordingly, PKCε ASO- and saline-treated mice were fed high-fat control or ethanol (EtOH)-containing enteral diets for 4 weeks.

Results

Chronic EtOH exposure significantly elevated hepatic lipid pools as well as activated PKCε. The PKCε ASO partially blunted the increases in hepatic lipids caused by E

SUBMITTER: Kaiser JP 

PROVIDER: S-EPMC4157371 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature