Hepatocyte-specific activity of TSC22D4 triggers progressive NAFLD by impairing mitochondrial function.

ABSTRACT:

Objective

Fibrotic organ responses have recently been identified as long-term complications in diabetes. Indeed, insulin resistance and aberrant hepatic lipid accumulation represent driving features of progressive non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis and non-alcoholic steatohepatitis (NASH) to fibrosis. Effective pharmacological regimens to stop progressive liver disease are still lacking to-date.

Methods

Based on our previous discovery of transforming growth factor beta-like stimulated clone (TSC)22D4 as a key driver of insulin resistance and glucose intolerance in obesity and type 2 diabetes, we generated a TSC22D4-hepatocyte specific knockout line (TSC22D4-HepaKO) and exposed mice to control or NASH diet models. Mechanistic insights wer

SUBMITTER: Wolff G 

PROVIDER: S-EPMC9034319 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature