Cardiomyocyte-specific deficiency of ketone body metabolism promotes accelerated pathological remodeling.

ABSTRACT:

Objective

Exploitation of protective metabolic pathways within injured myocardium still remains an unclarified therapeutic target in heart disease. Moreover, while the roles of altered fatty acid and glucose metabolism in the failing heart have been explored, the influence of highly dynamic and nutritionally modifiable ketone body metabolism in the regulation of myocardial substrate utilization, mitochondrial bioenergetics, reactive oxygen species (ROS) generation, and hemodynamic response to injury remains undefined.

Methods

Here we use mice that lack the enzyme required for terminal oxidation of ketone bodies, succinyl-CoA:3-oxoacid CoA transferase (SCOT) to determine the role of ketone body oxidation in the myocardial injury response. Tracer delivery in ex vivo perfused h

SUBMITTER: Schugar RC 

PROVIDER: S-EPMC4209361 | biostudies-literature | 2014 Oct

REPOSITORIES: biostudies-literature