In a patient with von Gierke disease, excessive hepatic glucose production is primarily due to:

The correct answer is C: Increased gluconeogenesis compensating for glucose-6-phosphatase deficiency. Von Gierke disease (GSD Type I) involves glucose-6-phosphatase deficiency, leading to impaired glucose release. However, alternative glucose production through gluconeogenesis and pentose phosphate pathway increases.

Which of the following enzymes requires a metal cofactor for its catalytic activity in the citric acid cycle?

The correct answer is A: Aconitase (requires Fe-S cluster). Aconitase requires an iron-sulfur cluster [4Fe-4S] for catalyzing the isomerization of citrate to isocitrate. This is essential for its catalytic mechanism in the TCA cycle.

A protein exhibits a β-sheet structure rich in proline residues. Why is this structurally problematic?

The correct answer is A: Proline lacks a free NH group to form backbone hydrogen bonds in β-sheets. Proline is an imino acid with its side chain bonded to the backbone nitrogen, eliminating the NH group needed for β-sheet hydrogen bonding between strands. High proline content disrupts β-sheet formation, commonly found in turns and loops instead.

Which statement best describes the relationship between glycogen structure and its metabolic advantages?

The correct answer is B: Branched structure with α-1,6-bonds increases solubility and accessibility to enzymes, enabling rapid glucose release. Glycogen's highly branched structure with α-1,6-branch points every 8-12 glucose residues increases its solubility, provides multiple substrate sites for glycogen phosphorylase simultaneously, and enables rapid glucose mobilization during energy demands. This is metabolically superior to linear poly

Which of the following describes cooperative binding in enzymes?

The correct answer is A: Binding of substrate increases affinity for subsequent substrates. Cooperative binding (positive cooperativity) occurs when binding of one substrate molecule enhances the affinity of the enzyme for additional substrate molecules, as seen in hemoglobin and phosphofructokinase.

Home

Home › Subjects › Biochemistry › Lipids

Biochemistry
Lipids

Metabolic pathways, enzymes, proteins

22 Q 3 Topics Take Mock Test

Difficulty: All Easy Medium Hard 1–10 of 22

Topics in Biochemistry

All Proteins & Enzymes 100 Carbohydrates 100 Lipids 78

Q.1 Hard Lipids

A patient with severely elevated serum triglycerides (>1000 mg/dL) is at immediate risk of:

A Only hypercholesterolemia

B Acute pancreatitis

C Peripheral neuropathy

D Myocardial infarction only

Correct Answer: B. Acute pancreatitis

EXPLANATION

Severe hypertriglyceridemia (>1000 mg/dL) significantly increases the risk of acute pancreatitis due to pancreatic inflammation caused by triglyceride-rich lipoproteins.

Test

Q.2 Hard Lipids

In the condition of hypertriglyceridemia with normal LDL levels, which genetic defect is most likely?

A LDL receptor deficiency

B Lipoprotein lipase or apoC-II deficiency

C CETP deficiency

D ApoB gene mutation

Correct Answer: B. Lipoprotein lipase or apoC-II deficiency

EXPLANATION

Deficiency of lipoprotein lipase or its cofactor apoC-II results in severe hypertriglyceridemia with elevated chylomicrons and VLDL but relatively normal LDL levels.

Test

Q.3 Hard Lipids

Tangier disease is associated with deficiency of which protein?

A ApoA-I

B ABCA1 transporter

C Lipoprotein lipase

D ApoB-100

Correct Answer: B. ABCA1 transporter

EXPLANATION

Tangier disease results from mutations in the ABCA1 gene, which encodes a cholesterol transporter. This leads to severe HDL deficiency and accumulation of cholesterol esters in tissues.

Test

Q.4 Hard Lipids

A patient presents with neurodegenerative symptoms, progressive neuropathy, and xanthomas. Plasma cholestanol and cholestane-3-beta,5-alpha,6-beta-triol levels are markedly elevated. Which genetic defect is most likely?

A ABCA1 mutation

B CYP27A1 mutation (sterol 27-hydroxylase deficiency)

C LCAT deficiency

D SREBP-2 mutation

Correct Answer: B. CYP27A1 mutation (sterol 27-hydroxylase deficiency)

EXPLANATION

CYP27A1 mutations cause cerebrotendinous xanthomatosis (CTX), characterized by elevated cholestanol and cholestane triol precursors due to impaired side-chain oxidation of cholesterol. This leads to progressive neurological deterioration, cataracts, and diarrhea. Chenodeoxycholic acid therapy is beneficial.

Test

Q.5 Hard Lipids

A 35-year-old patient with atherosclerosis has normal LDL cholesterol but elevated lipoprotein(a). Which genetic polymorphism is primarily responsible for high Lp(a) levels?

A APOE gene variations

B LPA gene variations affecting apo(a) size

C LDLR gene mutations

D PCSK9 gene polymorphisms

Correct Answer: B. LPA gene variations affecting apo(a) size

EXPLANATION

Lipoprotein(a) levels are predominantly determined by genetic variations in the LPA gene, which encodes apolipoprotein(a). Smaller isoforms are associated with higher plasma Lp(a) levels and increased cardiovascular risk, independent of LDL cholesterol levels.

Test

Q.6 Hard Lipids

A deficiency of apolipoprotein B-48 synthesis would primarily affect which lipid transport pathway?

A Cholesterol esterification

B Chylomicron formation and dietary lipid absorption

C HDL-mediated reverse cholesterol transport

D LDL receptor-mediated endocytosis

Correct Answer: B. Chylomicron formation and dietary lipid absorption

EXPLANATION

ApoB-48 is the truncated form of apoB synthesized in intestinal enterocytes and is essential for chylomicron assembly and secretion. Its deficiency causes abetalipoproteinemia, characterized by fat malabsorption and severe deficiency of fat-soluble vitamins.

Test

Q.7 Hard Lipids

During the fed state, acetyl-CoA carboxylase (ACC) is activated by which mechanism?

A Allosteric activation by AMP

B Phosphorylation by AMPK

C Phosphorylation by insulin-activated PKA

D Allosteric activation by citrate and phosphorylation by PKB/Akt

Correct Answer: D. Allosteric activation by citrate and phosphorylation by PKB/Akt

EXPLANATION

In the fed state, high citrate levels allosterically activate ACC, and insulin signaling causes PKB/Akt to phosphorylate and activate ACC. This promotes fatty acid synthesis. Conversely, AMPK phosphorylation inactivates ACC during energy deprivation.

Test

Q.8 Hard Lipids

A patient with primary biliary cholangitis shows elevated cholestanol levels. Which enzyme defect is most likely responsible?

A Sterol 7-alpha-hydroxylase

B Sterol 27-hydroxylase

C HMG-CoA reductase

D ACAT

Correct Answer: B. Sterol 27-hydroxylase

EXPLANATION

Sterol 27-hydroxylase catalyzes the side-chain oxidation of cholesterol to form bile acid precursors. Its deficiency or dysfunction leads to cholestanol accumulation and neuropathy. Elevated cholestanol is a characteristic finding in sterol 27-hydroxylase deficiency.

Test

Q.9 Hard Lipids

In Type III hyperlipoproteinemia (Familial Dysbetalipoproteinemia), the primary defect involves:

A Apolipoprotein E2 isoform with impaired receptor binding

B LDL receptor deficiency

C Lipoprotein lipase deficiency

D ABCA1 transporter mutation

Correct Answer: A. Apolipoprotein E2 isoform with impaired receptor binding

EXPLANATION

Type III hyperlipoproteinemia results from apoE2 homozygosity combined with another genetic or environmental factor. ApoE2 has reduced affinity for lipoprotein receptors, impairing remnant particle clearance.

Test

Q.10 Hard Lipids

The oxidative stress marker oxidized LDL (oxLDL) primarily activates which receptor to promote foam cell formation?

A LDL receptor

B SR-A (Scavenger receptor A) and LOX-1 (Lectin-like oxidized LDL receptor-1)

C HDL receptor

D ApoE receptor

Correct Answer: B. SR-A (Scavenger receptor A) and LOX-1 (Lectin-like oxidized LDL receptor-1)

EXPLANATION

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.

Test

1 2 3

All Subjects & Topics

Govt. Exams

Entrance Exams

Teacher Exams

Subjects

Quick Links

Biochemistry Lipids

Biochemistry
Lipids