Abnormal cardiac metabolism is responsible for the development of diabetic cardiomyopathy, identified in up to 70% of people with type 2 diabetes. However, understanding the mechanisms that cause increased cardiac fat metabolism leading to contractile dysfunction have remained elusive.
In a newly published paper, scientists have identified a new metabolic axis, whereby the cardiac fat transport CD36 becomes stuck at the plasma membrane in diabetes due to post-translation S-acylation. The research shows that pharmacologically targeting the enzymes regulating S-acylation can reverse the metabolic dysfunction and restore cardiac function in diabetes. As plasma membrane CD36 is the metabolic gatekeeper influencing all intracellular pathways utilising or regulated by fatty acids, this work paves the way toward the development of new cardiometabolic therapies in diabetes.
Read the full story on the Department of Physiology, Anatomy and Genetics website