NEET-PG 2012 - Biochemistry Practice Questions

Q: All are activated by insulin except?

Hormone sensitive lipase. ***Hormone sensitive lipase*** - **Insulin** is an **anabolic hormone** that promotes energy storage; it **inhibits** hormone-sensitive lipase (HSL) activity which is responsible for **fat breakdown (lipolysis)**. - When insulin levels are high, the body stores fat rather than breaks it down, thus **decreasing** HSL activity. *Lipoprotein lipase* - **Insulin activates lipoprotein lipase (LPL)**, an enzyme that breaks down triglycerides in **chylomicrons** and **VLDL** into fatty acids for storage in adipose tissue. - This activation promotes the uptake of fatty acids into fat cells, aligning with insulin's role in **energy storage**. *Pyruvate kinase* - **Insulin activates pyruvate kinase** in glycolysis, promoting the conversion of **phosphoenolpyruvate to pyruvate**. - This enzyme's activation enhances glucose utilization and energy production following a meal when insulin levels are high. *Acetyl-CoA carboxylase* - **Insulin activates acetyl-CoA carboxylase (ACC)**, the **rate-limiting enzyme in fatty acid synthesis**. - Activation of ACC leads to the production of **malonyl-CoA**, which commits acetyl-CoA to fatty acid synthesis, storing excess energy as fat.

Q: ATP is consumed at which of the following steps of glycolysis?

Hexokinase. ***Hexokinase*** - This enzyme catalyzes the **first step of glycolysis**, the phosphorylation of glucose to **glucose-6-phosphate**, which requires the consumption of one molecule of **ATP**. - ATP is hydrolyzed to **ADP**, providing the necessary phosphate group and energy for this irreversible reaction. - Note: Hexokinase is one of **two ATP-consuming steps** in glycolysis (the other being phosphofructokinase in step 3). *Pyruvate kinase* - This enzyme catalyzes the **final step of glycolysis**, converting **phosphoenolpyruvate (PEP)** to pyruvate. - This reaction involves the **production of ATP** from ADP, not its consumption, as it's one of the substrate-level phosphorylation steps. *Isomerase* - Isomerase enzymes, like phosphoglucose isomerase, convert one isomer to another (e.g., glucose-6-phosphate to fructose-6-phosphate). - These reactions generally involve an **internal rearrangement of atoms** and do not directly consume or produce ATP. *Enolase* - Enolase catalyzes the reversible conversion of **2-phosphoglycerate to phosphoenolpyruvate (PEP)**, releasing a molecule of water. - This step occurs before the ATP-generating step catalyzed by pyruvate kinase and **does not consume or produce ATP**.

Q: Glycogen synthase is activated by?

Insulin. **Insulin** - Insulin activates **glycogen synthase** through a signaling cascade that dephosphorylates the enzyme, shifting it to its active form (glycogen synthase a). - This activation promotes **glycogen synthesis** in the liver and muscles, lowering blood glucose levels. *Glucagon* - **Glucagon** primarily acts to increase blood glucose levels by activating **glycogen phosphorylase** and inhibiting glycogen synthase. - It promotes the breakdown of glycogen (glycogenolysis) rather than its synthesis. *Epinephrine* - **Epinephrine** (adrenaline) also promotes **glycogenolysis** (glycogen breakdown) by activating glycogen phosphorylase. - Its main role is to provide rapid energy during stress, not to store glucose as glycogen. *AMP* - **AMP** (adenosine monophosphate) is a key allosteric activator of **AMP-activated protein kinase (AMPK)**, which phosphorylates and inactivates glycogen synthase. - High AMP levels signal a low energy state, prompting ATP-generating pathways like glycogenolysis, not glycogen synthesis.

Q: What coenzyme is required by gulonate dehydrogenase for its activity?

NAD. ***NAD*** - **Gulonate dehydrogenase** is an enzyme involved in the **uronic acid pathway**, specifically in the conversion of **L-gulonate to D-xylulose**. - This reaction is an **NAD-dependent oxidation**, meaning **NAD** acts as the electron acceptor, being reduced to **NADH**. *NADP* - **NADP** (nicotinamide adenine dinucleotide phosphate) is primarily involved in **anabolic pathways** like **fatty acid synthesis** and the **pentose phosphate pathway**, often in reduction reactions where it is converted to **NADPH**. - While structurally similar to NAD, it is generally not the direct coenzyme for gulonate dehydrogenase. *FAD* - **FAD** (flavin adenine dinucleotide) is a coenzyme derived from **riboflavin** (vitamin B2) and is typically involved in **redox reactions** where it repeatedly accepts and donates electrons, often in dehydrogenase reactions involving **carbon-carbon double bonds**. - Enzymes like **succinate dehydrogenase** (in the citric acid cycle) or acyl-CoA dehydrogenase (in fatty acid oxidation) utilize FAD, but not gulonate dehydrogenase. *FMN* - **FMN** (flavin mononucleotide) is another coenzyme derived from **riboflavin** and serves as a prosthetic group in various **flavoproteins**, often facilitating **single-electron transfers**. - It is frequently found in complexes like **NADH dehydrogenase** (Complex I of the electron transport chain) but is not the required coenzyme for gulonate dehydrogenase activity.

Q: What is the rate-controlling enzyme of fatty acid synthesis?

Acetyl-CoA carboxylase. ***Acetyl-CoA carboxylase*** - **Acetyl-CoA carboxylase (ACC)** catalyzes the committed step in fatty acid synthesis, converting **acetyl-CoA** to **malonyl-CoA**. - This enzyme is subject to both allosteric regulation (e.g., activation by **citrate** and inhibition by **long-chain fatty acyl-CoA**) and hormonal regulation (e.g., phosphorylation by glucagon and dephosphorylation by insulin). *Thioesterase* - **Thioesterase** is the enzyme responsible for releasing the completed fatty acid chain from the **fatty acid synthase complex**. - While essential for the termination of synthesis, it does not regulate the initiation or overall rate of the pathway. *Transacetylase* - **Transacetylase** (specifically, acetyl-CoA-ACP transacetylase and malonyl-CoA-ACP transacetylase) is involved in transferring acetyl and malonyl groups to the **acyl carrier protein (ACP)** within the fatty acid synthesis complex. - This is an intermediary step, but not the primary **rate-controlling** or committed step. *Ketoacyl synthase* - **Ketoacyl synthase (or β-ketoacyl-ACP synthase)** is responsible for condensing the growing acyl chain with malonyl-ACP, leading to the formation of a **β-ketoacyl-ACP**. - This is a crucial chain elongation step within the fatty acid synthase complex, but not the enzyme that controls the overall commitment to fatty acid synthesis.

Q: Which of the following enzymes uses citrate in fatty acid synthesis?

ATP citrate lyase. ***ATP citrate lyase*** - This enzyme is crucial for fatty acid synthesis, as it cleaves **citrate** in the cytoplasm to generate **acetyl-CoA** and oxaloacetate. - The acetyl-CoA produced is then used as the primary building block for **fatty acid synthesis**. *Aconitase* - This enzyme isomerizes **citrate** to isocitrate within the **Krebs cycle** (TCA cycle) in the mitochondria. - It does not directly participate in the cytosolic pathway of fatty acid synthesis. *Citrate synthase* - This enzyme synthesizes **citrate** from acetyl-CoA and oxaloacetate, initiating the **Krebs cycle** in the mitochondrial matrix. - It is involved in citrate formation, not its utilization for fatty acid synthesis in the cytoplasm. *Malic enzyme* - This enzyme converts **malate** to pyruvate, generating **NADPH** in the cytoplasm. - While NADPH is essential for fatty acid synthesis, malic enzyme does not directly use citrate.

Q: Which of the following is an ω-6 fatty acid?

Linoleic acid. ***Linoleic acid*** - **Linoleic acid** (LA), an 18-carbon fatty acid with two double bonds (18:2), is classified as an **ω-6 fatty acid** because its first double bond is located at the sixth carbon atom from the methyl end of the fatty acid chain. - It is an **essential fatty acid** that must be obtained through diet, serving as a precursor for other ω-6 fatty acids like arachidonic acid. *Cervonic acid* - **Cervonic acid** is another name for **docosahexaenoic acid (DHA)**, which is an **ω-3 fatty acid** (22:6). - Its first double bond is located at the third carbon from the methyl end. *Alpha linolenic acid* - **Alpha-linolenic acid** (ALA) is an **ω-3 fatty acid** (18:3). - Its first double bond is located at the third carbon atom from the methyl end. *Elaidic acid* - **Elaidic acid** is a **trans fatty acid** (18:1 trans-9). - It is classified as an **ω-9 fatty acid** due to the position of its double bond, but its trans configuration is the primary distinguishing feature.

Q: Apo-E deficiency is seen in which of the following conditions?

Type III hyperlipoproteinemia. ***Type III hyperlipoproteinemia*** - This condition, also known as **familial dysbetalipoproteinemia** or **broad beta disease**, is characterized by a deficiency or abnormal function of **apolipoprotein E (apoE)**. - The deficiency in functional apoE impairs the clearance of **chylomicron remnants** and **intermediate-density lipoproteins (IDLs)** from the blood. *Type II hyperlipoproteinemia* - This condition primarily involves elevated **LDL cholesterol** and is often due to defects in the **LDL receptor** or mutations in **apoB-100**, not apoE deficiency. - It does not directly involve the impaired clearance of chylomicron remnants or IDLs. *Type I hyperlipoproteinemia* - Also known as **familial chylomicronemia syndrome**, this condition is characterized by severe elevation of **chylomicrons** and **triglycerides**. - It is caused by a deficiency of **lipoprotein lipase (LPL)** or its cofactor **apoC-II**, not apoE. *Type IV hyperlipoproteinemia* - This condition, also known as **familial hypertriglyceridemia**, is characterized by abnormally high levels of **very-low-density lipoproteins (VLDL)** and **triglycerides**. - It is typically caused by increased VLDL production or impaired VLDL clearance, but not directly due to an apoE deficiency.

Q: Which of the following is a lipotropic factor?

Methionine. ***Methionine*** - **Methionine** is an essential amino acid that serves as a precursor for **choline** and **creatine**, both of which play crucial roles in lipid metabolism and transport. - Lipotropic factors prevent or reverse the accumulation of **fat in the liver** by promoting the synthesis of **lipoproteins**, which package and transport fats from the liver to other tissues. *Sphingomyelin* - **Sphingomyelin** is a type of **sphingolipid**, a component of cell membranes and myelin sheaths, but it does not directly act as a lipotropic factor to prevent fatty liver. - While it's involved in cellular signaling and membrane structure, it does not directly facilitate the metabolism or transport of **hepatic triglycerides** in the same way as lipotropic agents. *Histidine* - **Histidine** is an essential amino acid involved in protein synthesis and the production of **histamine**, but it is not considered a primary lipotropic factor. - Its main roles are in **immune response** and **neurotransmission**, not in preventing fat accumulation in the liver. *Bilirubin* - **Bilirubin** is a waste product from the breakdown of **heme**, primarily from red blood cells. It is excreted by the liver. - It is known for its **antioxidant properties** but does not play a direct role as a lipotropic factor in lipid metabolism or in preventing **fatty liver**.

Q: Which enzyme deficiency is responsible for Hyperammonemia type-1?

Carbamoyl phosphate synthetase I (CPS-1) deficiency. ***Carbamoyl phosphate synthetase I (CPS-1) deficiency*** - This enzyme deficiency is classified as **Hyperammonemia type-1**, or **CPS1 deficiency**, and results in the inability to initiate the urea cycle. - **CPS-1** catalyzes the first committed step of the urea cycle, combining ammonia and bicarbonate to form carbamoyl phosphate. *Arginase deficiency* - This deficiency causes **Hyperargininemia**, which is a disorder of the urea cycle distinct from Hyperammonemia type-1. - Arginase is involved in the final step of the urea cycle, converting arginine to urea and ornithine. *Arginosuccinate lyase deficiency* - This deficiency leads to **Argininosuccinic aciduria**, another urea cycle disorder. - **Arginosuccinate lyase** is responsible for breaking down argininosuccinate into arginine and fumarate. *Arginosuccinate synthase deficiency* - This deficiency causes **Citrullinemia type 1**, a metabolic disorder characterized by high levels of citrulline and ammonia. - **Arginosuccinate synthase** catalyzes the condensation of citrulline and aspartate to form argininosuccinate.

Question 1

All are activated by insulin except?

Accepted Answer

Hormone sensitive lipase

Answer

Lipoprotein lipase

Answer

Pyruvate kinase

Answer

Acetyl-CoA carboxylase

Question 2

ATP is consumed at which of the following steps of glycolysis?

Accepted Answer

Hexokinase

Answer

Pyruvate kinase

Answer

Isomerase

Answer

Enolase

Question 3

Glycogen synthase is activated by?

Accepted Answer

Insulin

Answer

Glucagon

Answer

AMP

Answer

Epinephrine

Question 4

What coenzyme is required by gulonate dehydrogenase for its activity?

Accepted Answer

NAD

Answer

FAD

Answer

FMN

Answer

NADP

Question 5

What is the rate-controlling enzyme of fatty acid synthesis?

Accepted Answer

Acetyl-CoA carboxylase

Answer

Thioesterase

Answer

Transacetylase

Answer

Ketoacyl synthase

Question 6

Which of the following enzymes uses citrate in fatty acid synthesis?

Accepted Answer

ATP citrate lyase

Answer

Aconitase

Answer

Malic enzyme

Answer

Citrate synthase

Question 7

Which of the following is an ω-6 fatty acid?

Accepted Answer

Linoleic acid

Answer

Cervonic acid

Answer

Alpha linolenic acid

Answer

Elaidic acid

Question 8

Apo-E deficiency is seen in which of the following conditions?

Accepted Answer

Type III hyperlipoproteinemia

Answer

Type II hyperlipoproteinemia

Answer

Type I hyperlipoproteinemia

Answer

Type IV hyperlipoproteinemia

Question 9

Which of the following is a lipotropic factor?

Accepted Answer

Methionine

Answer

Sphingomyelin

Answer

Histidine

Answer

Bilirubin

Question 10

Which enzyme deficiency is responsible for Hyperammonemia type-1?

Accepted Answer

Carbamoyl phosphate synthetase I (CPS-1) deficiency

Answer

Arginase deficiency

Answer

Arginosuccinate lyase deficiency

Answer

Arginosuccinate synthase deficiency

NEET-PG 2012 — Biochemistry