Govt Exams
OxLDL is recognized by scavenger receptors (SR-A and LOX-1) on macrophages, not by the classical LDL receptor. This leads to unregulated cholesterol uptake and foam cell formation in atherosclerosis.
Thyroid hormones upregulate LDL receptors and also inhibit HMG-CoA reductase. In hypothyroidism, all these effects are reversed, leading to increased cholesterol levels through multiple mechanisms.
Lp(a) levels are primarily determined by genetic factors (LPA gene polymorphisms) and are elevated in chronic kidney disease due to reduced catabolism. Lp(a) is an independent cardiovascular risk factor.
CPT-I is allosterically inhibited by malonyl-CoA, a key regulatory point linking fatty acid synthesis (high during fed state) with fatty acid oxidation (low during fed state).
Tangier disease results from mutations in ABCA1 gene, which encodes an ATP-binding cassette transporter essential for HDL biogenesis. This leads to severe HDL deficiency and cholesterol accumulation in tissues.
Small, dense LDL particles (Pattern B) are more atherogenic because they penetrate arterial walls more easily, are more susceptible to oxidation, and have reduced hepatic clearance compared to large, buoyant LDL particles.
Insulin activates mTORC1, which promotes protein synthesis and lipogenesis. It also increases acetyl-CoA carboxylase activity, promoting fatty acid synthesis from carbohydrate sources.
Niemann-Pick Type C results from mutations in NPC1 or NPC2 genes, which encode lysosomal cholesterol transporters, leading to lysosomal accumulation of cholesterol and sphingolipids.
ApoB-100 is essential for the structural integrity and secretion of VLDL and LDL particles. It remains with these particles throughout their metabolism.
Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are synthesized primarily in the liver mitochondria during periods of high fatty acid oxidation.