Cholesterol Synthesis, Transport and Excretion MCQs

Gα S- activates adenylyl cyclase Adenylyl cyclase is the enzyme responsible for formation of CAMP So, if there is Gα S , there is increase in production of cAMP Reference: Ganong 25th edition page No.57

Highest level of GLUT1 is present in the RBC Major Glucose transporter in brain is GLUT1 (not present in neurons) Major Glucose transporter in the Placenta is GLUT 1 Major Glucose transporter in the RBC is GLUT1 Major neuronal Glucose transporter is GLUT3 Insulin-responsive glucose transporter is GLUT4, GLUT 8 and GLUT 12 Fructose transporter GLUT 5 (mainly) and GLUT 11 Urate transporter is GLUT 9 Glucose transporter in blastocyst is GLUT 8. Reference : Harper's 32 nd edition, Page no. 191

Explanation: Lipotropic factors are substances that promote the export of fat from the liver, preventing hepatic steatosis (fatty liver). Choline , lecithin (which contains choline), and methionine (which can be converted to cysteine and is a methyl donor) are classic lipotropic agents, arginine is not.( Option A,B and D ruled out) Arginine is primarily involved in the urea cycle, nitric oxide synthesis, and other metabolic pathways unrelated to hepatic lipid transport. Key Takeaways: Lipotropic factors prevent fatty liver (e.g., choline, methionine, betaine, inositol). Arginine is not a lipotropic factor.

HMG CoA is utilised in the following reactions: Ketogenesis: Formation of HMG CoA from three molecules of acetyl CoA by the enzyme HMGCoA synthase which is the rate limiting step of ketogenesis Cholesterol synthesis: HMG CoA is converted to Mevalonate by the enzyme HMGCoA reductase which is the rate limiting step of Cholesterol synthesis Leucine metabolism: HMG CoA is an intermediate in leucine catabolism Reference: Harper's illustrated biochemistry 32 nd edition, page no 525, 718

Hepatic lipase degrades TG's in IDL Hormone sensitive lipase degrades TG's in adipocytes Lipoprotein lipase degrades TG's circulating Chylomicrons and VLDLs in the vascular endothelium Pancreatic lipase degrades TG's in the small intestine Reference: Harper's illustrated biochemistry 32 nd edition page 604

Ans. is 'b i.e., Hormone sensitive lipase [Ref : Harper 29th/e chap. 16] Adipose tissue fat (TGs) metabolism → Hormone sensitive lipase Lipoproteins (VLDL & chylomicrons) TGs metabolism - Lipoprotein lipase

Disease:- Familial type III hyperlipoproteinemia (broad beta disease, remnant removal disease, familial dysbetalipoproteinemia) Defect:- Deficiency in remnant clearance by the liver is due to abnormality in apo E. Patients lack isoforms E3 and E4 and have only E2, which does not react with the E receptor Remarks:- Increase in chylomicron and VLDL remnants of density Reference: Harper's illustrated biochemistry 32 nd edition, page 275

Explanation: Hormone-Sensitive Lipase (HSL): HSL breaks down stored triglycerides in adipose tissue into free fatty acids and glycerol. In diabetes, HSL activity is increased , releasing more free fatty acids into circulation, which the liver uses to synthesize VLDL (Very Low-Density Lipoprotein). Lipoprotein Lipase (LPL): LPL hydrolyzes triglycerides in VLDL and chylomicrons into free fatty acids for tissue uptake. In diabetes, LPL activity is reduced , impairing the clearance of VLDL from the bloodstream. Combined Effect: High HSL → more substrate for hepatic VLDL production. Low LPL → reduced VLDL clearance. Result: elevated VLDL levels in diabetic patients, contributing to hypertriglyceridemia. Hence options B,C, and D are incorrect