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BI4.1-8 | Chemistry and Metabolism of Lipids — Gate Quiz
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Arachidonic acid (20:4) is an omega-6 fatty acid. What does omega-6 signify?
Correct! Omega-6 means the first double bond is at carbon 6 from the methyl terminus.
Essential fatty acids: Omega-6 (linoleic acid) and Omega-3 (alpha-linolenic acid) cannot be synthesized by humans. Arachidonic acid (omega-6) is precursor to prostaglandins and leukotrienes.
Incorrect. Omega designation specifies the position of the first double bond from the methyl end.
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During beta-oxidation of palmitic acid (16:0, saturated), how many cycles of beta-oxidation are required to fully oxidize it?
Correct! A 16-carbon fatty acid requires 7 cycles to produce 8 acetyl-CoA units. Cycles = (carbons/2) - 1 = 8 - 1 = 7.
Beta-oxidation: each cycle removes 2 carbons as acetyl-CoA and produces 1 NADH + 1 FADH2. Palmitate (C16): 7 cycles = 8 acetyl-CoA + 7 NADH + 7 FADH2. Total yield approximately 106 ATP.
Incorrect. For a 16-carbon fatty acid: 7 cycles produce 8 acetyl-CoA. Formula: cycles = (carbons/2) - 1.
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Ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are synthesized in which organ?
Correct! Ketone bodies are exclusively synthesized in hepatic mitochondria from acetyl-CoA, primarily during fasting or diabetic ketoacidosis.
Liver produces ketone bodies when acetyl-CoA exceeds TCA capacity. The liver cannot use its own ketone bodies (lacks thiophorase). During DKA, blood ketones cause acidosis.
Incorrect. Ketogenesis occurs only in liver mitochondria.
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A Type 1 diabetic patient presents with fruity breath, Kussmaul respiration, and blood ketones of 8 mmol/L. The main reason for excessive ketogenesis is:
Correct! Insulin deficiency: unregulated lipolysis causes excess FFA, liver beta-oxidation generates excess acetyl-CoA, gluconeogenesis depletes oxaloacetate, so acetyl-CoA is diverted to ketogenesis.
DKA mechanism: Insulin deficiency increases hormone-sensitive lipase (lipolysis), massive FFA release, hepatic beta-oxidation, excess acetyl-CoA. Gluconeogenesis consumes OAA, blocking TCA cycle, so acetyl-CoA goes to ketone bodies.
Incorrect. Insulin deficiency causes unregulated lipolysis plus excess acetyl-CoA plus OAA depletion leading to ketogenesis.
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The key regulatory enzyme of fatty acid synthesis that is activated by insulin and inhibited by glucagon is:
Correct! Acetyl-CoA carboxylase (ACC) is the rate-limiting enzyme of fatty acid synthesis, catalyzing acetyl-CoA to malonyl-CoA. Activated by citrate and insulin; inhibited by glucagon/epinephrine.
ACC regulation: Activated by citrate (allosteric) and insulin (dephosphorylation); Inhibited by palmitoyl-CoA, glucagon/epinephrine (via cAMP-PKA-phosphorylation = inactive). Malonyl-CoA also inhibits CPT-I, preventing beta-oxidation during fed state.
Incorrect. Acetyl-CoA carboxylase (ACC) is the committed, rate-limiting step of fatty acid synthesis.
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The rate-limiting enzyme of cholesterol synthesis that is the target of statin drugs is:
Correct! HMG-CoA reductase catalyzes HMG-CoA to mevalonate, the rate-limiting step of cholesterol synthesis. Statins are competitive inhibitors of this enzyme.
Cholesterol synthesis: Acetyl-CoA to HMG-CoA to (HMG-CoA reductase) Mevalonate to Squalene to Lanosterol to Cholesterol. Statins lower LDL by inhibiting HMG-CoA reductase, which upregulates LDL receptors on hepatocytes.
Incorrect. HMG-CoA reductase is the rate-limiting enzyme targeted by statins.
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A 50-year-old man has elevated LDL-C (180 mg/dL). LDL transports cholesterol from:
Correct! LDL (Low Density Lipoprotein) delivers cholesterol from liver to peripheral tissues. LDL is the main atherogenic lipoprotein.
Lipoprotein transport: Chylomicrons = dietary lipids from intestine to periphery. VLDL = liver triglycerides to periphery. LDL = cholesterol from liver to tissues (atherogenic). HDL = reverse cholesterol transport, periphery to liver (protective).
Incorrect. LDL transports cholesterol from liver to peripheral tissues.
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Aspirin inhibits cyclooxygenase (COX) irreversibly. This reduces synthesis of which eicosanoids from arachidonic acid?
Correct! COX is required for prostaglandin and thromboxane synthesis. Aspirin inhibits COX, blocking these products. Leukotrienes use lipoxygenase, which aspirin does not inhibit.
Arachidonic acid metabolism: COX pathway produces prostaglandins + thromboxanes. LOX pathway produces leukotrienes. In aspirin-sensitive asthma, shunting to LOX pathway increases leukotrienes.
Incorrect. COX produces prostaglandins and thromboxanes. Leukotrienes use lipoxygenase, unaffected by aspirin.
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Tay-Sachs disease is caused by deficiency of hexosaminidase A. The accumulated substrate is:
Correct! Hexosaminidase A deficiency prevents degradation of GM2 ganglioside, which accumulates in neurons causing progressive neurodegeneration.
Sphingolipid storage diseases: Tay-Sachs (hexosaminidase A, GM2), Gaucher (glucocerebrosidase, glucocerebroside), Niemann-Pick (sphingomyelinase, sphingomyelin), Krabbe (galactocerebrosidase, galactocerebroside). All AR except Fabry (X-linked).
Incorrect. Hexosaminidase A cleaves GM2 ganglioside; its deficiency causes GM2 accumulation.
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Pancreatic lipase hydrolyzes dietary triglycerides. The main products absorbed by intestinal cells are:
Correct! Pancreatic lipase preferentially hydrolyzes the sn-1 and sn-3 positions, producing 2 free fatty acids and 1 2-monoglyceride.
Lipid digestion: Emulsification by bile salts then pancreatic lipase (with colipase) cleaves sn-1,3 positions. Products absorbed by enterocytes, resynthesized to TG, packaged as chylomicrons, secreted into lacteals.
Incorrect. Pancreatic lipase acts at sn-1 and sn-3 positions producing 2 FFAs + 1 2-monoglyceride.
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