Entrance Exams
Govt. Exams
ApoA-I is the major apolipoprotein of HDL, essential for LCAT activation and cholesterol esterification, promoting reverse cholesterol transport and HDL maturation.
Palmitate (C16) undergoes 7 cycles of beta-oxidation producing 8 acetyl-CoA molecules, 7 FADH2, and 7 NADH. Total ATP yield is approximately 129 ATP (accounting for initial activation cost).
Lipoprotein lipase deficiency causes Type I hyperlipoproteinemia with severe accumulation of chylomicrons and triglycerides (>1000 mg/dL), risk of acute pancreatitis.
Epinephrine and glucagon activate hormone-sensitive lipase via cAMP signaling in adipose tissue, promoting lipolysis and release of free fatty acids during fasting or stress.
High triglycerides with low HDL is characteristic of metabolic syndrome, often associated with insulin resistance, obesity, and increased cardiovascular risk.
The liver is the primary site of lipogenesis, where excess carbohydrates and amino acids are converted to fatty acids and triglycerides for storage and export via VLDL.
Cortisol and other corticosteroids are synthesized from cholesterol in the adrenal cortex through a series of enzymatic reactions involving cytochrome P450 enzymes.
Excessive dietary saturated fat increases liver production of VLDL, which carries triglycerides and cholesterol. VLDL is converted to LDL in circulation, raising LDL levels.
Phospholipids have a glycerol backbone with two fatty acids and a phosphate group, making them amphipathic. This structure is crucial for membrane formation.
HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate, the rate-limiting and key regulatory step in cholesterol biosynthesis. It is targeted by statin drugs.