Abstract
Presentation Description :
Tissues with high metabolic rates often use lipid as well as glucose for energy, conferring a survival advantage during feast and famine. Current dogma suggests that high-energy consuming photoreceptors depend on glucose. However, we found that retina also uses fatty acid β-oxidation for energy. Lipid sensors curb glucose uptake when fatty acids are available. Impaired glucose entry into photoreceptors results in a dual lipid/glucose fuel shortage and reduction in the Krebs cycle intermediate α-ketoglutarate (KG) to promote hypoxia- induced factor-1α stabilization and vascular endothelial growth factor secretion, attracting neovessels to supply fuel. Dysregulated lipid and glucose photoreceptor energy metabolism may therefore be a driving force in neovascular retinal diseases.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.