Biochemistry
9 questionsWhich of the following statements about NADP is correct?
In the malate shuttle, how many ATPs are produced from one NADH?
Which of the following is not a substrate for gluconeogenesis?
Pyruvate dehydrogenase requires all cofactors except:
Which of the following processes primarily utilizes lactate produced anaerobically?
Citrate synthase is inhibited by -
Fumarate is formed from which amino acid?
Enzyme deficient in Hers disease -
Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 271: Which of the following statements about NADP is correct?
- A. Involved in fatty acid oxidation
- B. Involved in HMP shunt (Correct Answer)
- C. Involved in glycolysis
- D. Acts as a coenzyme form of Riboflavin
Explanation: ***Involved in HMP shunt*** - **NADPH**, the reduced form of NADP+, is primarily generated in the **hexose monophosphate shunt (HMP shunt)**, specifically during the oxidative phase. - The NADPH produced in the HMP shunt is crucial for **reductive biosynthesis** reactions and maintaining the **redox balance** of the cell. *Acts as a coenzyme form of Riboflavin* - **NADP is derived from Niacin (Vitamin B3)**, not Riboflavin (Vitamin B2). - **Flavin adenine dinucleotide (FAD)** and **flavin mononucleotide (FMN)** are the coenzyme forms of Riboflavin. *Involved in glycolysis* - **NADP is not directly involved in glycolysis**; instead, **NAD+** is the primary coenzyme that accepts electrons in glycolysis, specifically during the oxidation of glyceraldehyde-3-phosphate. - While some enzymes in glycolysis can interact with NADP+ under specific conditions, its main role is not within the glycolytic pathway. *Involved in fatty acid oxidation* - **Fatty acid oxidation (beta-oxidation)** primarily utilizes **NAD+** and **FAD** as electron acceptors. - **NADP+** is not a direct participant in the electron transport chain during fatty acid breakdown.
Question 272: In the malate shuttle, how many ATPs are produced from one NADH?
- A. 1 ATP
- B. 3 ATP
- C. 2 ATP
- D. 2.5 ATP (Correct Answer)
Explanation: ***2.5 ATP*** - In the **malate-aspartate shuttle**, mitochondrial **NADH** is regenerated from cytosolic NADH, and then enters the electron transport chain at **Complex I**. - **Complex I** entry means that NADH contributes to the pumping of enough protons to generate approximately **2.5 ATP** through oxidative phosphorylation. *1 ATP* - **1 ATP** is not the direct equivalent produced from the reoxidation of one NADH via the malate shuttle into the electron transport chain. - This value is typically associated with the direct hydrolysis of **ATP** or the energy equivalent of **GTP** produced in the citric acid cycle. *3 ATP* - Historically, **3 ATP** was the accepted stoichiometry for one NADH, but more accurate measurements of proton pumping and ATP synthase activity have revised this. - The value of 3 ATP per NADH does not reflect the most current understanding of mitochondrial bioenergetics. *2 ATP* - **2 ATP** is the approximate yield for **FADH2** entering the electron transport chain at **Complex II**, bypassing Complex I, and thus pumping fewer protons. - This value is not applicable to NADH transferred via the malate-aspartate shuttle, as NADH enters at Complex I.
Question 273: Which of the following is not a substrate for gluconeogenesis?
- A. Leucine (Correct Answer)
- B. Lactate
- C. Propionate
- D. Glycerol
Explanation: ***Leucine*** - **Leucine** is an exclusively **ketogenic amino acid**, meaning its breakdown products can only be converted into **ketone bodies** or fatty acids, not glucose. - It does not have a carbon skeleton that can be directly converted into **pyruvate** or **oxaloacetate**, which are key intermediates in gluconeogenesis. *Lactate* - **Lactate** is a major substrate for gluconeogenesis, particularly during exercise or fasting. - It is converted to **pyruvate** by **lactate dehydrogenase**, and pyruvate can then enter the gluconeogenic pathway. *Propionate* - **Propionate** is a fatty acid with an odd number of carbon atoms, primarily derived from the catabolism of odd-chain fatty acids or from bacterial fermentation in the colon. - It can be converted into **succinyl CoA**, an intermediate of the citric acid cycle, which can then be used for gluconeogenesis. *Glycerol* - **Glycerol**, released during the breakdown of triglycerides, is an important substrate for gluconeogenesis. - It is phosphorylated to **glycerol-3-phosphate**, which is then oxidized to **dihydroxyacetone phosphate (DHAP)**, an intermediate in glycolysis and gluconeogenesis.
Question 274: Pyruvate dehydrogenase requires all cofactors except:
- A. Thiamin
- B. Pyridoxin (Vitamin B6) (Correct Answer)
- C. Riboflavin
- D. Niacin
Explanation: ***Pyridoxin (Vitamin B6)*** - **Pyridoxin** (vitamin B6) is a coenzyme for many enzymes involved in **amino acid metabolism**, but it is **not directly required** by the pyruvate dehydrogenase complex. - The pyruvate dehydrogenase complex uses **thiamine pyrophosphate**, **lipoic acid**, **FAD**, **NAD+**, and **Coenzyme A** as cofactors. *Thiamin* - **Thiamin pyrophosphate** (TPP), derived from thiamin (vitamin B1), is a crucial coenzyme for the **E1 subunit** of the pyruvate dehydrogenase complex. - It participates in the **decarboxylation** of pyruvate, releasing CO2. *Riboflavin* - **FAD** (flavin adenine dinucleotide), derived from riboflavin (vitamin B2), is a coenzyme for the **E3 subunit** (dihydrolipoyl dehydrogenase) of the pyruvate dehydrogenase complex. - It is involved in the **regeneration of oxidized lipoamide**. *Niacin* - **NAD+** (nicotinamide adenine dinucleotide), derived from niacin (vitamin B3), is a coenzyme for the **E3 subunit** of the pyruvate dehydrogenase complex. - It acts as an **electron acceptor** during the reoxidation of FADH2.
Question 275: Which of the following processes primarily utilizes lactate produced anaerobically?
- A. Cori cycle (Correct Answer)
- B. Gluconeogenesis
- C. TCA cycle
- D. Glycolysis
Explanation: ***Cori cycle*** - The **Cori cycle** (lactic acid cycle) involves the transport of **lactate** produced during anaerobic metabolism in muscles to the liver. - In the **liver**, this lactate is then converted back to **glucose** via gluconeogenesis, which can be returned to the muscles. *Gluconeogenesis* - **Gluconeogenesis** is the synthesis of glucose from non-carbohydrate precursors, one of which is lactate. - While it uses lactate, it is only one component of the broader **Cori cycle**, which describes the inter-organ cooperation. *Glycolysis* - **Glycolysis** is the metabolic pathway that breaks down glucose into pyruvate, which can then be converted to lactate under anaerobic conditions. - This process *produces* lactate but does not *utilize* it, acting upstream of lactate production. *TCA cycle* - The **TCA cycle** (Krebs cycle) is a central part of aerobic respiration that oxidizes acetyl-CoA to produce ATP, NADH, and FADH2. - It does not directly utilize lactate; instead, lactate is typically converted to pyruvate before potentially entering the TCA cycle under aerobic conditions.
Question 276: Citrate synthase is inhibited by -
- A. Insulin
- B. Glucagon
- C. ADP
- D. ATP (Correct Answer)
Explanation: ***ATP*** - **Citrate synthase**, a key enzyme in the Krebs cycle, is inhibited by **high levels of ATP**, indicating a high energy state in the cell. - This allosteric inhibition helps regulate the metabolic flux through the cycle, slowing it down when energy is abundant. *ADP* - **ADP** typically signifies a low energy state and would generally act as an **activator** rather than an inhibitor for metabolic pathways that produce ATP. - In this context, ADP would promote the activity of enzymes involved in energy generation, including those in the Krebs cycle. *Insulin* - **Insulin** is a hormone that promotes fuel storage and utilization, generally **activating** metabolic pathways rather than directly inhibiting enzymes like citrate synthase. - Its primary role is to regulate blood glucose levels and promote glucose uptake and utilization. *Glucagon* - **Glucagon** is a hormone that mobilizes fuel from storage and is typically associated with **catabolic processes**, often increasing metabolic activity in response to low blood glucose. - It does not directly inhibit citrate synthase; its main actions are on glucoregulation.
Question 277: Fumarate is formed from which amino acid?
- A. Methionine
- B. Valine
- C. Histidine
- D. Tyrosine (Correct Answer)
Explanation: ***Tyrosine*** - **Tyrosine** is a **glucogenic and ketogenic amino acid** that is catabolized to acetoacetate and fumarate. - **Fumarate** then enters the **citric acid cycle (Krebs cycle)**, whereas acetoacetate is a ketone body. *Methionine* - **Methionine** is an **essential amino acid** and a precursor for **S-adenosylmethionine (SAM)**, a methyl donor in many reactions. - Its catabolism produces **succinyl CoA**, not fumarate, through a series of steps via propionyl CoA. *Valine* - **Valine** is a **branched-chain amino acid (BCAA)** that is exclusively **glucogenic**. - Its catabolism ultimately leads to the formation of **succinyl CoA**, which can enter the citric acid cycle. *Histidine* - **Histidine** is an **essential amino acid** that is catabolized to **formiminoglutamate (FIGLU)**. - FIGLU is then converted to **glutamate**, which can eventually be deaminated to α-ketoglutarate, a citric acid cycle intermediate, but not directly fumarate.
Question 278: Enzyme deficient in Hers disease -
- A. Muscle phosphorylase
- B. Liver phosphorylase (Correct Answer)
- C. Acid maltase
- D. Debranching enzyme
Explanation: ***Liver phosphorylase*** - Hers disease, also known as Glycogen Storage Disease Type VI, is specifically caused by a deficiency of **liver phosphorylase**. - This enzyme is crucial for the breakdown of **glycogen in the liver**, leading to an inability to release glucose into the bloodstream during fasting. *Muscle phosphorylase* - Deficiency of **muscle phosphorylase** (myophosphorylase) causes **McArdle disease** (Glycogen Storage Disease Type V), which primarily affects muscle energy. - Patients typically present with exercise intolerance, muscle pain, and cramps, not the hepatic symptoms seen in Hers disease. *Acid maltase* - Deficiency of **acid maltase** (also known as alpha-glucosidase) is responsible for **Pompe disease** (Glycogen Storage Disease Type II), a lysosomal storage disorder. - This enzyme deficiency leads to glycogen accumulation in lysosomes in various tissues, including muscle, liver, and heart, causing muscle weakness and cardiomyopathy. *Debranching enzyme* - A deficiency in the **debranching enzyme** (amylo-1,6-glucosidase) causes **Cori disease** or **Forbes disease** (Glycogen Storage Disease Type III). - This results in the accumulation of abnormally structured glycogen with short outer branches in the liver, muscle, and heart.
Question 279: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
- A. Glucokinase is induced by insulin. (Correct Answer)
- B. Hexokinase is specific for glucose.
- C. Glucokinase is inhibited by glucose-6-phosphate.
- D. Hexokinase has a high Km for glucose.
Explanation: ***Glucokinase is induced by insulin.*** - **Insulin** promotes glucose uptake and utilization in the liver and pancreatic beta cells, where glucokinase is primarily expressed. - Induction of **glucokinase** by insulin ensures that glucose is efficiently phosphorylated and trapped within hepatocytes when blood glucose levels are high. - This is a key mechanism for postprandial glucose homeostasis. *Incorrect: Hexokinase is specific for glucose.* - **Hexokinase** is NOT specific for glucose; it can phosphorylate various hexoses including **fructose**, **mannose**, and **galactose**. - Its broad substrate specificity distinguishes it from glucokinase, which has greater specificity for glucose. *Incorrect: Glucokinase is inhibited by glucose-6-phosphate.* - Unlike **hexokinase**, which is subject to product inhibition by glucose-6-phosphate, **glucokinase is NOT inhibited** by its product. - This lack of feedback inhibition allows glucokinase to continue phosphorylating glucose even when glucose-6-phosphate levels are elevated, which is appropriate for its role as a glucose sensor in liver and pancreatic beta cells. *Incorrect: Hexokinase has a high Km for glucose.* - **Hexokinase** has a **low Km** (~0.1 mM) for glucose, meaning it has high affinity and is saturated at normal blood glucose levels. - In contrast, **glucokinase** has a high Km (~10 mM), allowing it to respond proportionally to changes in blood glucose concentration.
Physiology
1 questionsThe major role of 2,3-bisphosphoglycerate in RBCs is -
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 271: The major role of 2,3-bisphosphoglycerate in RBCs is -
- A. Acid-base balance
- B. Reversal of glycolysis
- C. Release of oxygen (Correct Answer)
- D. Binding of oxygen
Explanation: ***Release of oxygen*** - **2,3-bisphosphoglycerate (2,3-BPG)** binds allosterically to **deoxyhemoglobin**, stabilizing its T (tense) state. - This binding reduces hemoglobin's affinity for oxygen, promoting the **release of oxygen** to tissues. *Acid-base balance* - While red blood cells play a role in **acid-base balance** through the bicarbonate buffer system, 2,3-BPG's primary role is not buffering. - The **chloride shift** and **carbonic anhydrase** are more directly involved in RBC acid-base regulation. *Reversal of glycolysis* - 2,3-BPG is an intermediate of the **Rapoport-Luebering shunt**, a side pathway of glycolysis. - It does not reverse glycolysis but rather is produced during glycolysis to serve a specific function in oxygen transport. *Binding of oxygen* - 2,3-BPG **decreases** hemoglobin's affinity for oxygen, thus promoting its *release* from hemoglobin, not its binding. - Oxygen binding to hemoglobin occurs primarily at the **heme iron** without 2,3-BPG.