What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
What is the role of nonsense codons in protein synthesis?
Which hormone is known to repress the biosynthesis of the enzyme pyruvate carboxylase?
Which molecule serves as a key link between carbohydrate metabolism and fatty acid synthesis?
Which carbohydrate is primarily metabolized by Aldolase-B?
Which vitamin is involved in one-carbon transfer reactions?
Which of the following statements about chylomicrons is true?
Which enzyme is primarily responsible for the fat metabolism in adipose tissue?
Enzyme deficient in Type I Hyperlipidemia?
Which of the following pairs of compounds has the highest standard reduction potential?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 41: What is the net number of ATP molecules and NADH formed in glycolysis per glucose molecule?
- A. 4 ATP, 2 NADH
- B. 4 ATP, 4 NADH
- C. 2 ATP, 4 NADH
- D. 2 ATP, 2 NADH (Correct Answer)
Explanation: **2 ATP, 2 NADH** - Glycolysis has a net yield of **2 molecules of ATP** because 4 ATP molecules are produced, but 2 ATP molecules are consumed during the initial energy investment phase. - **2 molecules of NADH** are also produced during the energy generation phase when glyceraldehyde-3-phosphate is oxidized. *4 ATP, 2 NADH* - While 4 ATP molecules are indeed produced during glycolysis, this option does not account for the **2 ATP molecules consumed** in the initial steps, leading to an incorrect net value. - The production of **2 NADH** is correct, but the ATP count is the gross rather than the net. *4 ATP, 4 NADH* - This option overstates the production of both ATP and NADH. While **4 ATP are produced (gross)**, the net is 2 ATP. - Only **2 NADH** molecules are formed per glucose molecule in glycolysis, not 4. *2 ATP, 4 NADH* - This option accurately reflects the **net ATP yield of 2 molecules**. - However, it exaggerates the production of NADH, as only **2 molecules of NADH** are formed during glycolysis, not 4.
Question 42: What is the role of nonsense codons in protein synthesis?
- A. Elongation of the polypeptide chain
- B. Pre-translational modification of proteins
- C. Initiation of protein synthesis
- D. Termination of protein synthesis (Correct Answer)
Explanation: ***Termination of protein synthesis*** - **Nonsense codons**, also known as **stop codons** (UAA, UAG, UGA), signal the end of translation. - When a ribosome encounters a nonsense codon, it binds **release factors** instead of an aminoacyl-tRNA, leading to the dissociation of the polypeptide chain. *Elongation of the polypeptide chain* - **Elongation** involves the sequential addition of amino acids to the growing polypeptide chain, guided by sense codons. - Nonsense codons do not code for any amino acid and thus do not contribute to chain elongation. *Pre-translational modification of proteins* - **Pre-translational modifications** refer to events like protein folding and disulfide bond formation that occur as the polypeptide is being synthesized. - Nonsense codons are involved in halting the synthesis, not in modifying the protein. *Initiation of protein synthesis* - **Initiation** of protein synthesis begins at the **start codon** (AUG), which codes for methionine. - Nonsense codons are distinct from the start codon and fulfill a different role in the translation process.
Question 43: Which hormone is known to repress the biosynthesis of the enzyme pyruvate carboxylase?
- A. Cortisol
- B. Glucagon
- C. Insulin (Correct Answer)
- D. Growth hormone
Explanation: ***Insulin*** - **Insulin** is an anabolic hormone that promotes glucose utilization and opposes **gluconeogenesis**. - While insulin does inhibit hepatic glucose production, it primarily acts by **repressing PEPCK (phosphoenolpyruvate carboxykinase)**, the rate-limiting enzyme of gluconeogenesis, rather than directly repressing pyruvate carboxylase biosynthesis. - **Note:** Modern biochemistry emphasizes that insulin's main transcriptional target in gluconeogenesis is **PEPCK**, not pyruvate carboxylase. However, this was the expected answer for **NEET-2012**, reflecting the understanding at that time. - Insulin also promotes dephosphorylation and inactivation of gluconeogenic enzymes and enhances glucose uptake and glycolysis. *Glucagon* - **Glucagon** is a catabolic hormone that **activates** enzymes involved in **gluconeogenesis** and glycogenolysis to raise blood glucose levels. - It would **increase**, not repress, the biosynthesis and activity of gluconeogenic enzymes including **pyruvate carboxylase**. *Cortisol* - **Cortisol** is a glucocorticoid hormone that **stimulates gluconeogenesis** in the liver as part of the stress response. - It typically **upregulates** the synthesis and activity of gluconeogenic enzymes like **pyruvate carboxylase** and **PEPCK**. *Growth hormone* - **Growth hormone** generally **increases insulin resistance** and can have a **diabetogenic effect**, promoting glucose production rather than repressing gluconeogenic enzymes. - It does not directly repress gluconeogenic enzyme biosynthesis; its metabolic effects favor lipolysis and protein synthesis.
Question 44: Which molecule serves as a key link between carbohydrate metabolism and fatty acid synthesis?
- A. Glucose-6-phosphate
- B. Acetyl-CoA
- C. Citrate (Correct Answer)
- D. Succinyl-CoA
Explanation: ***Citrate*** - **Citrate** is the crucial molecule that links carbohydrate metabolism to fatty acid synthesis via the **citrate-malate shuttle** - In the fed state, excess **acetyl-CoA** (derived from glucose metabolism via glycolysis and pyruvate dehydrogenase) condenses with oxaloacetate to form citrate in the mitochondria - **Citrate** is then transported from mitochondria to the cytosol, where **ATP-citrate lyase** cleaves it to regenerate **acetyl-CoA** and **oxaloacetate** for fatty acid synthesis - This is the primary mechanism for transporting acetyl-CoA equivalents from mitochondria (where glucose is oxidized) to the cytosol (where fatty acids are synthesized) - Citrate also acts as an **allosteric activator** of **acetyl-CoA carboxylase**, the rate-limiting enzyme of fatty acid synthesis *Glucose-6-phosphate* - While **glucose-6-phosphate** is a key intermediate in glycolysis and gluconeogenesis, it is not the molecule that directly links carbohydrate breakdown to fatty acid synthesis - It is several steps removed from the generation of cytosolic acetyl-CoA needed for fatty acid synthesis *Acetyl-CoA* - **Acetyl-CoA** is the direct precursor for fatty acid synthesis - However, acetyl-CoA generated in mitochondria from glucose oxidation **cannot directly cross the mitochondrial membrane** - It must be transported as citrate, making citrate the actual linking molecule between the two compartments *Succinyl-CoA* - **Succinyl-CoA** is a Krebs cycle intermediate involved in heme synthesis and propionate metabolism - It is not involved in transporting acetyl units from mitochondria to cytosol for fatty acid synthesis
Question 45: Which carbohydrate is primarily metabolized by Aldolase-B?
- A. Galactose
- B. Fructose (Correct Answer)
- C. Sucrose
- D. None of the options
Explanation: ***Fructose*** - **Aldolase B** is a key enzyme in the liver responsible for the metabolism of **fructose**, specifically cleaving **fructose-1-phosphate** into **dihydroxyacetone phosphate** and **glyceraldehyde**. - A deficiency in **Aldolase B** leads to **hereditary fructose intolerance**, causing an accumulation of **fructose-1-phosphate** after fructose ingestion. *Galactose* - **Galactose** is primarily metabolized by enzymes in the **Leloir pathway**, including **galactokinase** and **galactose-1-phosphate uridylyltransferase**. - **Aldolase B** plays no significant role in the metabolism of galactose. *Sucrose* - **Sucrose** is a disaccharide composed of **glucose** and **fructose**. - It is first broken down by **sucrase** in the small intestine into its constituent monosaccharides before they are metabolized further. *None of the options* - This option is incorrect because **fructose** is indeed a carbohydrate primarily metabolized by Aldolase-B. - The enzyme's specific role in fructose metabolism is well-established.
Question 46: Which vitamin is involved in one-carbon transfer reactions?
- A. Folic acid (Correct Answer)
- B. Pantothenic acid
- C. Niacin
- D. Thiamine
Explanation: ***Folic acid*** - **Folic acid (Vitamin B9)** is a crucial coenzyme in the form of **tetrahydrofolate (THF)**, which acts as a carrier of **one-carbon units**. - These one-carbon units are essential for various metabolic pathways, including the synthesis of **purines**, **thymidylate**, and the metabolism of several **amino acids**. *Pantothenic acid* - **Pantothenic acid (Vitamin B5)** is a precursor to **Coenzyme A (CoA)**, which plays a central role in fatty acid metabolism and the **Krebs cycle**, not one-carbon transfers. - CoA is involved in transferring **acetyl groups**, not one-carbon units. *Niacin* - **Niacin (Vitamin B3)** is a component of **NAD+** and **NADP+**, which are vital coenzymes in **redox reactions** (electron transfer), not one-carbon metabolism. - It functions primarily in **energy metabolism** as an electron carrier. *Thiamine* - **Thiamine (Vitamin B1)** is a coenzyme for **dehydrogenase reactions** and **transketolase** in the **pentose phosphate pathway**, which are involved in carbohydrate metabolism. - It does not directly participate in one-carbon transfer reactions.
Question 47: Which of the following statements about chylomicrons is true?
- A. Chylomicrons are unrelated to triglyceride transport.
- B. Chylomicrons primarily contain cholesterol.
- C. Chylomicrons primarily contain triglycerides (TGs). (Correct Answer)
- D. Chylomicrons do not primarily contain triglycerides.
Explanation: ***Chylomicrons primarily contain triglycerides (TGs)*** - **Chylomicrons** are the largest and least dense lipoproteins, primarily responsible for transporting **dietary triglycerides** absorbed from the intestine to peripheral tissues. - They are synthesized in the **enterocytes** of the small intestine and released into the lymphatic system. - Approximately **85-90%** of a chylomicron's mass is composed of **triglycerides**, making them the primary carriers of exogenous fats. *Chylomicrons primarily contain cholesterol* - While chylomicrons do contain some **cholesterol**, it is a minor component (~3-5%) compared to their predominant content, which is **triglycerides**. - Lipoproteins like **LDL** and **HDL** are primarily responsible for cholesterol transport. *Chylomicrons are unrelated to triglyceride transport* - This statement is incorrect; chylomicrons are fundamentally involved in the **transport of dietary triglycerides** from the intestines to various tissues in the body. - After lipoprotein lipase acts on chylomicrons in peripheral tissues, triglycerides are hydrolyzed and fatty acids are taken up by tissues. *Chylomicrons do not primarily contain triglycerides* - This statement directly contradicts the main function and composition of chylomicrons, which are **rich in triglycerides**. - Without triglycerides as their primary content, chylomicrons would not be able to fulfill their physiological role in lipid transport.
Question 48: Which enzyme is primarily responsible for the fat metabolism in adipose tissue?
- A. Lipoprotein lipase
- B. Hormone-sensitive lipase (Correct Answer)
- C. Acid lipase
- D. Acid maltase
Explanation: ***Hormone-sensitive lipase*** - This enzyme is crucial for the **mobilization of stored triglycerides** in adipose tissue by hydrolyzing them into fatty acids and glycerol. - Its activity is stimulated by hormones like **epinephrine** and **norepinephrine** and inhibited by insulin, reflecting its role in regulating fat release during energy demand. *Lipoprotein lipase* - This enzyme is primarily located on the **endothelial surface of capillaries** in various tissues, including adipose tissue, muscle, and heart. - Its main role is to clear **triglyceride-rich lipoproteins** like chylomicrons and VLDL from the bloodstream, facilitating the uptake of fatty acids into cells for storage or energy, rather than direct fat metabolism within the adipose cell. *Acid lipase* - **Lysosomal acid lipase** functions within lysosomes to break down cholesterol esters and triglycerides that are taken up by cells. - Its primary role is in the degradation of lipids within the **lysosomal compartments**, not in the primary process of fat mobilization from adipose tissue stores. *Acid maltase* - Also known as **alpha-glucosidase**, this enzyme is a lysosomal enzyme responsible for breaking down glycogen into glucose. - Its function is related to **glycogen metabolism** and has no direct role in fat metabolism in adipose tissue.
Question 49: Enzyme deficient in Type I Hyperlipidemia?
- A. HMG CoA reductase
- B. Lipoprotein lipase (Correct Answer)
- C. Peroxidase
- D. Cholesterol acyl transferase
Explanation: ***Lipoprotein lipase*** - **Type I hyperlipidemia**, also known as **familial hyperchylomicronemia**, is characterized by a deficiency in **lipoprotein lipase (LPL)**. - LPL is crucial for hydrolyzing triglycerides in **chylomicrons** and **VLDLs** into fatty acids and glycerol, allowing their uptake by tissues. *HMG CoA reductase* - This enzyme is involved in the **rate-limiting step of cholesterol synthesis** in the liver. - While it plays a role in lipid metabolism, its deficiency is not characteristic of **Type I hyperlipidemia**. *Peroxidase* - **Peroxidase** is an enzyme involved in various oxidative reactions, including the breakdown of **hydrogen peroxide**. - It is not directly involved in the metabolism of **chylomicrons** or **triglycerides**, and its deficiency is unrelated to hyperlipidemia. *Cholesterol acyl transferase* - This enzyme, often referring to **lecithin-cholesterol acyltransferase (LCAT)** or **acyl-CoA:cholesterol acyltransferase (ACAT)**, is involved in **cholesterol esterification**. - While important for cholesterol transport and storage, its deficiency is not the primary cause of **Type I hyperlipidemia**, which is marked by severe **chylomicronemia**.
Question 50: Which of the following pairs of compounds has the highest standard reduction potential?
- A. NADH/NAD+
- B. Succinate/Fumarate
- C. Ubiquinone/Ubiquinol
- D. Fe³⁺/Fe²⁺ (Correct Answer)
Explanation: ***Fe³⁺/Fe²⁺*** - The **Fe³⁺/Fe²⁺ couple** has a **standard reduction potential (E'0)** of **+0.77 V**, making it the highest among the given options. - A higher positive E'0 indicates a stronger tendency for the oxidized form to accept electrons and be reduced. *NADH/NAD+* - The **NADH/NAD+ couple** has a **standard reduction potential** of **-0.32 V**, indicating it is a strong reducing agent. - Its negative reduction potential means it readily donates electrons during metabolic processes. *Succinate/Fumarate* - The **succinate/fumarate couple** has a **standard reduction potential** of **+0.03 V**. - This pair is involved in the **TCA cycle**, where succinate is oxidized to fumarate, releasing electrons. *Ubiquinone/Ubiquinol* - The **ubiquinone/ubiquinol couple** has a **standard reduction potential** varying around **+0.05 to +0.10 V**, depending on the specific state. - It acts as a mobile electron carrier in the **electron transport chain**, accepting electrons from NADH and FADH2.