Practice question

Neutral lipid storage avoiding lipotoxicity requires chemical conversion free cholesterol hydrophobic ester for sequestration in droplets. ACAT SOAT enzymes ER catalyze transfer oleate oleoyl CoA three beta hydroxyl cholesterol forming cholesteryl oleate no polar head logP about fifteen versus cholesterol logP eight increasing hydrophobicity dramatically. Completely apolar molecule partitions oil phase lipid droplet core together triacylglycerol lens that buds droplet surrounded phospholipid monolayer perilipins PLIN. Esterification sequesters cholesterol away regulatory ER pool sensed SCAP INSIG SREBP preventing ER stress unfolded protein response apoptosis. Hydrolysis NCEH1 LIPE hormone sensitive lipase restores free cholesterol membrane repair steroidogenesis bile acid synthesis liver intestine. Sphingomyelin phosphatidylserine phosphatidylethanolamine remain membrane phospholipids amphipathic heads not stored neutral oil core. Excess cholesteryl ester accumulation macrophages via ACAT1 produces foam cells hallmark atherosclerosis plaques tendon xanthomas familial hypercholesterolemia leading myocardial infarction stroke. Understanding ester storage links cholesterol homeostasis metabolic disease pathobiology therapeutic targeting avasimibe ACAT inhibitors lipid droplet biology core cell biology cardiovascular pathology questions for exams and clinical correlations hyperlipidemia management.