Loss of MPC1 reprograms retinal metabolism to impair visual function

Abstract

Significance Mitochondrial pyruvate carrier (MPC) is responsible for transporting pyruvate from glycolysis into mitochondria for oxidative phosphorylation. In the vertebrate retinas, the majority of glucose is metabolized into lactate by glycolysis rather than being oxidized in the mitochondria. Here, we show that although a small percentage of glucose is transported through MPC, deletion of MPC impairs visual function, decreases the viability of photoreceptors, disrupts photoreceptor ultrastructure, and causes glial activation. We find that MPC is required for maintaining the retinal metabolism in amino acids, neurotransmitters, and ketone bodies.