Enhancing cardiac glycolysis causes an increase in PDK4 content in response to short-term high-fat diet.

ABSTRACT: The healthy heart has a dynamic capacity to respond and adapt to changes in nutrient availability. Metabolic inflexibility, such as occurs with diabetes, increases cardiac reliance on fatty acids to meet energetic demands, and this results in deleterious effects, including mitochondrial dysfunction, that contribute to pathophysiology. Enhancing glucose usage may mitigate metabolic inflexibility and be advantageous under such conditions. Here, we sought to identify how mitochondrial function and cardiac metabolism are affected in a transgenic mouse model of enhanced cardiac glycolysis (Glyco^Hi) basally and following a short-term (7-day) high-fat diet (HFD). Glyco^Hi mice constitutively express an active form of phosphofructokinase-2, resulting in elevated levels of the

SUBMITTER: Newhardt MF 

PROVIDER: S-EPMC6851294 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature