Alterations of hepatic ATP homeostasis and respiratory chain during development of non‐alcoholic steatohepatitis in a rodent model

Abstract

The loss of hepatic ATP stores is not dependent on the F(0)F(1)-ATPase but resides in the respiratory chain. Dysfunction of both Complex I and II of the mitochondrial respiratory chain during NASH development implies a mitochondrial adaptive mechanism occurring in the early stages of NASH.