Govt Exams
HDL has approximately 50% protein content, the highest among all lipoproteins. Chylomicrons and VLDL are triglyceride-rich lipoproteins with lower protein ratios.
Familial hypercholesterolemia presents with xanthomas due to defective LDL receptors. Type II hyperlipoproteinemia (IIa) is essentially familial hypercholesterolemia with elevated LDL. Both terms describe the same condition in this clinical context.
AMPK phosphorylates and inactivates acetyl-CoA carboxylase during energy stress (high AMP/ATP ratio), thereby reducing fatty acid synthesis. Citrate and insulin activate the enzyme.
Linoleic acid and alpha-linolenic acid are essential fatty acids that cannot be synthesized by humans and must be obtained from dietary sources.
HDL mediates reverse cholesterol transport, removing excess cholesterol from peripheral tissues and transporting it to the liver for excretion. High HDL levels are protective against cardiovascular disease.
Most fatty acids undergo beta-oxidation in the mitochondrial matrix. However, very long chain fatty acids (>20 carbons) are initially oxidized in peroxisomes.
Acetyl-CoA carboxylase catalyzes the formation of malonyl-CoA from acetyl-CoA, which is the first committed and rate-limiting step in fatty acid synthesis.
Triacylglycerols are storage lipids found primarily in adipose tissue. Phosphatidylcholine, cholesterol, and sphingomyelin are major components of cell membranes.
Xanthomas (lipid deposits in skin and tendons) and corneal arcus (lipid deposition in cornea) are hallmark signs of severe hypercholesterolemia, typically with very high LDL cholesterol levels.
Eicosanoid synthesis begins with phospholipase A2-mediated release of arachidonic acid (C20 polyunsaturated fatty acid) from membrane phospholipids, which then serves as substrate for COX and LOX pathways.