Hepatocyte-specific eNOS deletion impairs exercise-induced adaptations in hepatic mitochondrial function and autophagy.

ABSTRACT:

Objective

Endothelial nitric oxide synthase (eNOS) is a potential mediator of exercise-induced hepatic mitochondrial adaptations.

Methods

Here, male and female hepatocyte-specific eNOS knockout (eNOS^hep-/- ) and intact hepatic eNOS (eNOS^fl/fl ) mice performed voluntary wheel-running exercise (EX) or remained in sedentary cage conditions for 10 weeks.

Results

EX resolved the exacerbated hepatic steatosis in eNOS^hep-/- male mice. Elevated hydrogen peroxide emission (~50% higher in eNOS^hep-/- vs. eNOS^fl/fl mice) was completely ablated with EX. Interestingly, EX increased [1-¹⁴ C] palmitate oxidation in eNOS^fl/fl male mice, but this was blunted in the eNOS^hep-/- male mice. eNOS^hep

SUBMITTER: Cunningham RP 

PROVIDER: S-EPMC9050943 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature