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BIO CHEMISTRY QUIZLET — Full Answers & Explanations

Q1. Which set of GLUTs is not dependent on insulin?

✅ Answer: A — I, II, III (GLUT-1, GLUT-2, GLUT-3)

Explanation: GLUT-4 is the only glucose transporter that is insulin-dependent. In the presence of insulin, GLUT-4 translocates from intracellular vesicles to the cell membrane — this is the primary mechanism by which insulin lowers blood glucose in skeletal muscle and adipose tissue. GLUT-1, GLUT-2, and GLUT-3 are constitutively active (always present on the cell surface) and do NOT require insulin. So the set that is not insulin-dependent = GLUT-1, II, and III → Option A.

Lippincott Biochemistry 8e: "The glucose transporter (GLUT-4) in adipose and muscle tissue is dependent on insulin... The other [GLUTs] are not insulin dependent."

Q2. Lactase enzyme breaks?

✅ Answer: B — Beta 1,4 glycosidic bond

Explanation: Lactose is a disaccharide made of galactose + glucose linked by a β-1,4 glycosidic bond. Lactase (lactase-phlorizin hydrolase) is a brush-border enzyme in the small intestine that cleaves this bond to release free galactose and glucose for absorption. Lactase deficiency leads to lactose intolerance — undigested lactose is fermented by gut bacteria producing gas and osmotic diarrhea.

Q3. Increased ketone body production during prolonged fasting — what's responsible?

✅ Answer: C — Increased β-oxidation producing excess acetyl-CoA

Explanation: During prolonged fasting:

Insulin levels fall → glucagon rises
Adipose tissue releases free fatty acids (lipolysis)
Free fatty acids enter the liver and undergo β-oxidation, generating large amounts of acetyl-CoA
Oxaloacetate (OAA) is depleted (diverted to gluconeogenesis), so the TCA cycle cannot accept all the acetyl-CoA
Excess acetyl-CoA is shunted into ketogenesis → acetoacetate, β-hydroxybutyrate, and acetone (ketone bodies)

Options A, B, and D are wrong: insulin is decreased in fasting; OAA availability is reduced (not increased); and glycogen synthesis is suppressed during fasting.

Medical Physiology: "Accelerated β-oxidation of FAs produces acetyl-CoA faster than the [TCA cycle] can handle, leading to ketone body production."

Q4. Which process takes the longest during the fed state?

✅ Answer: D — Synthesis of new enzymes

Explanation: This is about the speed of metabolic regulation. From fastest to slowest:

Availability of substrates — immediate (milliseconds)
Allosteric activation/inhibition — seconds (conformational change)
Covalent modification (phosphorylation/dephosphorylation) — minutes
Synthesis of new enzymes (transcription + translation) — hours (the slowest)

Enzyme synthesis requires gene expression: transcription of mRNA, then translation into protein — this is the most time-consuming regulatory mechanism.

Q5. Which glucose transporter is insulin-sensitive and found in skeletal muscle and adipose tissue?

✅ Answer: D — GLUT-4

Explanation: GLUT-4 is the insulin-regulated transporter. At rest, GLUT-4 is sequestered in intracellular vesicles. When insulin binds its receptor, a signaling cascade (PI3K → Akt) causes these vesicles to fuse with the plasma membrane, massively increasing glucose uptake. This is the key mechanism of post-meal glucose clearance and the defect in type 2 diabetes.

Transporter	Location	Key Feature
GLUT-1	RBCs, brain, placenta	Basal glucose uptake
GLUT-2	Liver, pancreatic β-cells, small intestine	High Km, glucose sensor
GLUT-3	Brain, neurons	High affinity, low Km
GLUT-4	Skeletal muscle, adipose, heart	Insulin-dependent

Q6. What is cleaved from proinsulin in the Golgi apparatus?

✅ Answer: C — C-peptide

Explanation: Insulin synthesis follows this pathway:

Preproinsulin is synthesized on ribosomes → the signal sequence is cleaved in the ER
Proinsulin (A-chain + C-peptide + B-chain in one chain) folds and disulfide bonds form in the ER
In the Golgi apparatus / secretory granules, proteases (prohormone convertases PC1/PC2 + carboxypeptidase E) cleave out the C-peptide, yielding mature insulin (A-chain + B-chain connected by two disulfide bonds)

C-peptide is secreted equimolarly with insulin and is used clinically to assess endogenous insulin secretion (e.g., distinguishing type 1 diabetes from insulin injection).

Q7. During fasting, which pathway does glucagon stimulate to maintain blood glucose?

✅ Answer: C — Gluconeogenesis

Explanation: Glucagon is the "fasting hormone." It acts on the liver to:

Stimulate gluconeogenesis (making new glucose from amino acids, lactate, glycerol) ✅
Stimulate glycogenolysis (short-term glucose release)
Inhibit glycolysis, glycogenesis, and lipogenesis

Gluconeogenesis is the primary mechanism for maintaining blood glucose during prolonged fasting once glycogen stores are depleted.

Q8. Which combination correctly matches transporter and property?

✅ Answer: C — GLUT-4: insulin-dependent, found in muscle and adipose tissue

Explanation — why the others are wrong:

A (GLUT-2 high affinity, insulin-dependent) → WRONG. GLUT-2 has low affinity (high Km ~15–20 mM), acts as a glucose sensor, and is NOT insulin-dependent
B (GLUT-3 low affinity, bidirectional) → WRONG. GLUT-3 has high affinity (low Km ~1 mM) to serve the brain's constant glucose needs
C (GLUT-4 insulin-dependent, muscle/adipose) → CORRECT ✅
D (GLUT-1 only in liver) → WRONG. GLUT-1 is in RBCs, brain, placenta; GLUT-2 is the liver transporter

Q9. Normal cholesterol but extremely high triglycerides — which lipoprotein is elevated?

✅ Answer: D — VLDL

Explanation: Different lipoproteins carry different cargo:

Chylomicrons — carry dietary (exogenous) triglycerides from gut → periphery
VLDL — carry endogenous triglycerides synthesized in the liver → periphery
LDL — primarily carries cholesterol (derived from VLDL remnants)
HDL — reverse cholesterol transport

If cholesterol is normal but TGs are extremely elevated, the culprit is VLDL (endogenous pathway). Chylomicrons would also cause hypertriglyceridemia but only transiently after meals. In the clinical context of a fasting sample with chronically elevated TGs and normal cholesterol, VLDL is the primary suspect. (Note: very high chylomicrons post-meal can also raise TGs, but VLDL is the classic fasting answer for familial hypertriglyceridemia.)

Q10. Which compound is BOTH a precursor AND inhibitor in lipid metabolism?

✅ Answer: C — Malonyl-CoA

Explanation: Malonyl-CoA has a dual role:

Precursor: It is the 2-carbon donor in fatty acid synthesis. Acetyl-CoA carboxylase converts acetyl-CoA → malonyl-CoA, and fatty acid synthase (FAS) uses malonyl-CoA to elongate the growing fatty acid chain
Inhibitor: Malonyl-CoA inhibits CPT-I (carnitine palmitoyltransferase I), the enzyme that transports long-chain fatty acyl groups into the mitochondria for β-oxidation

This elegant reciprocal control ensures that fatty acid synthesis and β-oxidation do not occur simultaneously — when you're building fats (fed state), malonyl-CoA is high and blocks fat burning.

Lippincott Biochemistry 8e: "Malonyl CoA inhibits CPT-I, thus preventing the entry of long-chain acyl groups into the mitochondrial matrix. Therefore, when fatty acid synthesis is occurring...[β-oxidation is blocked]."

Q11. Chylomicrons transport dietary lipids from?

✅ Answer: B — Intestinal mucosal cells to peripheral tissues

Explanation: Chylomicrons are assembled in intestinal epithelial cells (enterocytes) from dietary fat absorbed in the small intestine. They are secreted into lacteals (lymph) → thoracic duct → enter the bloodstream at the subclavian vein → deliver triglycerides to peripheral tissues (muscle, adipose) via lipoprotein lipase on capillary walls. Chylomicron remnants are then taken up by the liver.

The other options describe different lipoprotein pathways (VLDL goes liver → periphery; free fatty acids from adipose → liver, bound to albumin).

Q12. The urea (ornithine) cycle takes place in which compartment?

✅ Answer: C — Both mitochondria and cytoplasm

Explanation: The urea cycle spans two compartments in hepatocytes:

Mitochondrial steps (steps 1–2):

NH₃ + CO₂ → Carbamoyl phosphate (by CPS-I)
Carbamoyl phosphate + ornithine → Citrulline (by OTC)

Citrulline exits the mitochondria via a transporter

Cytoplasmic steps (steps 3–5): 3. Citrulline + aspartate → Argininosuccinate 4. Argininosuccinate → Arginine + fumarate 5. Arginine → Urea + ornithine (by arginase)

Ornithine re-enters the mitochondria to continue the cycle

Basic Medical Biochemistry 6e: "The urea cycle spans two compartments: the mitochondria (where carbamoyl phosphate and citrulline are produced) and the cytoplasm (where the remainder of the cycle takes place)."

Answer Key Summary

Q	Answer	Topic
1	A (GLUT 1, 2, 3)	Insulin-independent GLUTs
2	B (β-1,4 bond)	Lactase substrate
3	C (β-oxidation → excess acetyl-CoA)	Ketogenesis in fasting
4	D (Enzyme synthesis)	Speed of metabolic regulation
5	D (GLUT-4)	Insulin-sensitive transporter
6	C (C-peptide)	Insulin processing
7	C (Gluconeogenesis)	Glucagon's fasting action
8	C (GLUT-4)	Transporter properties
9	D (VLDL)	Hypertriglyceridemia
10	C (Malonyl-CoA)	Precursor + inhibitor
11	B (Intestine → periphery)	Chylomicron transport
12	C (Mitochondria + cytoplasm)	Urea cycle compartments

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