Carbohydrate Metabolism — MCQs
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Which enzyme is primarily associated with the reduction of NADP+ to NADPH in the pentose phosphate pathway?
Which one of the following statements concerning gluconeogenesis is correct?
Which of the following is an amino sugar formed from fructose-6-phosphate?
Which of the following statements BEST describes the net ATP production in glycolysis?
Which glycogen storage disease also presents as a lysosomal storage disease?
Glucose is converted to glucuronate by which process?
Which of the following substances does not inhibit glycolysis?
What cofactor is required for the proper functioning of glucose-6-phosphate dehydrogenase?
Increased uric acid levels are seen in which glycogen storage disease ?
GLUT2 plays a functionally important role mainly in?
Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs
Question 761: Which enzyme is primarily associated with the reduction of NADP+ to NADPH in the pentose phosphate pathway?
- A. G6PD (Correct Answer)
- B. APDH
- C. α-keto glutarate dehydrogenases
- D. None of the options
Explanation: ***G6PD*** - **Glucose-6-phosphate dehydrogenase (G6PD)** catalyzes the first committed step in the pentose phosphate pathway, converting **glucose-6-phosphate** to **6-phosphogluconolactone**. - This reaction involves the reduction of **NADP+ to NADPH**, making G6PD the primary enzyme for NADPH production in this pathway. *APDH* - **APDH (adenosine phosphosulfate reductase)** is involved in sulfur metabolism and has no direct role in the pentose phosphate pathway or NADPH production. - This enzyme primarily functions in prokaryotes for the **reduction of APS (adenosine 5'-phosphosulfate)**. *α-keto glutarate dehydrogenases* - **Alpha-ketoglutarate dehydrogenase** is a mitochondrial enzyme part of the **Krebs cycle**, converting **alpha-ketoglutarate to succinyl-CoA**. - This enzyme is crucial for ATP production and generates **NADH**, not NADPH, in its reaction. *None of the options* - This option is incorrect because **G6PD** is indeed the primary enzyme responsible for NADPH generation in the pentose phosphate pathway.
Question 762: Which one of the following statements concerning gluconeogenesis is correct?
- A. It occurs primarily in the liver.
- B. It is stimulated by elevated levels of acetyl CoA.
- C. It is important in maintaining blood glucose during the normal overnight fast. (Correct Answer)
- D. It is primarily inhibited by insulin.
Explanation: ***It is important in maintaining blood glucose during the normal overnight fast.*** - **This is the BEST answer** as it emphasizes the **primary physiological role** of gluconeogenesis in human metabolism. - During the **overnight fast** (8-12 hours), hepatic glycogen stores become depleted, making gluconeogenesis the **critical mechanism** to maintain blood glucose for glucose-dependent tissues like the **brain** (requires ~120g glucose/day) and **red blood cells**. - Without gluconeogenesis, blood glucose would drop dangerously during fasting, leading to hypoglycemia and neurological dysfunction. *It occurs primarily in the liver.* - This statement is **technically correct** - the liver accounts for approximately **90%** of total gluconeogenesis under normal conditions. - However, the **kidney cortex** also contributes significantly (10% normally, up to 40% during prolonged fasting), and the **intestine** plays a minor role. - While true, this is more of a **anatomical fact** rather than highlighting the critical physiological importance of the pathway, making it a less comprehensive answer than Option 1. *It is stimulated by elevated levels of acetyl CoA.* - This statement is **biochemically correct** - **Acetyl-CoA** is an important **allosteric activator** of **pyruvate carboxylase**, the first committed enzyme of gluconeogenesis. - However, this represents just **one regulatory mechanism** at the enzymatic level, not the overall physiological significance. - Primary regulation occurs through **hormones** (glucagon, cortisol, epinephrine) that coordinate the entire pathway, making this a narrower answer than Option 1. *It is primarily inhibited by insulin.* - This statement is also **correct** - **Insulin** is the primary hormonal **inhibitor** of gluconeogenesis. - Insulin suppresses gluconeogenesis by inhibiting key enzymes (PEPCK, glucose-6-phosphatase) and decreasing transcription of gluconeogenic genes. - However, this describes **inhibition** rather than the positive physiological role, making it less representative of gluconeogenesis's essential function than Option 1. **Note:** All four statements are technically correct, but Option 1 best captures the **essential physiological importance** of gluconeogenesis in human metabolism, which is why it is the preferred answer for this question.
Question 763: Which of the following is an amino sugar formed from fructose-6-phosphate?
- A. N-acetylglucosamine-6-phosphate
- B. Glucosamine-6-phosphate (Correct Answer)
- C. Galactosamine-6-phosphate
- D. UDP-N-acetylglucosamine
Explanation: ***Glucosamine-6-phosphate*** - This amino sugar is directly synthesized from **fructose-6-phosphate** via a transamidation reaction, where an amino group replaces a hydroxyl group. - It is a key intermediate in the biosynthesis of other **amino sugars** and **glycosaminoglycans**. *N-acetylglucosamine-6-phosphate* - This is formed from **glucosamine-6-phosphate** by the addition of an **acetyl group**, making it a subsequent product, not the initial amino sugar from fructose-6-phosphate. - The N-acetylation step is crucial for its role in cellular signaling and structural components. *Galactosamine-6-phosphate* - While an amino sugar, **galactosamine-6-phosphate** is derived from UDP-N-acetylglucosamine, not directly from fructose-6-phosphate. - Its formation involves an **epimerization** step of an existing N-acetylglucosamine structure. *UDP-N-acetylglucosamine* - This is an **activated form** of N-acetylglucosamine, formed by the addition of UTP to N-acetylglucosamine-1-phosphate. - It serves as a precursor for the synthesis of complex **carbohydrates** and glycoproteins, far downstream from fructose-6-phosphate.
Question 764: Which of the following statements BEST describes the net ATP production in glycolysis?
- A. Glycolysis produces 2 molecules of pyruvate
- B. Glycolysis produces a net gain of 2 ATP per glucose molecule (Correct Answer)
- C. Hexokinase consumes ATP during glycolysis
- D. Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules
Explanation: ***Glycolysis produces a net gain of 2 ATP per glucose molecule*** - In the initial "investment" phase of glycolysis, **2 ATP molecules are consumed** to phosphorylate glucose. - In the subsequent "payoff" phase, **4 ATP molecules are produced** through substrate-level phosphorylation, resulting in a net gain of 2 ATP. *Glycolysis produces 2 molecules of pyruvate* - While glycolysis does produce **2 molecules of pyruvate** from one glucose molecule, this statement describes the end product of the pathway, not the net ATP production. - Pyruvate is a crucial product that can be further metabolized in aerobic or anaerobic conditions, but it does not directly represent the energy yield in terms of ATP. *Hexokinase consumes ATP during glycolysis* - **Hexokinase** is indeed the enzyme that catalyzes the first ATP-consuming step in glycolysis, phosphorylating glucose to glucose-6-phosphate. - However, this statement describes only one aspect of ATP utilization within the pathway and does not account for the total ATP produced or the overall net gain. *Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules* - **Aldolase** is a key enzyme in glycolysis responsible for cleaving **fructose-1,6-bisphosphate** into dihydroxyacetone phosphate and glyceraldehyde-3-phosphate. - This step is part of the preparatory phase of glycolysis but does not directly describe the net ATP production.
Question 765: Which glycogen storage disease also presents as a lysosomal storage disease?
- A. Von Gierke's disease
- B. McArdle's disease
- C. Andersen's disease
- D. Pompe's disease (Correct Answer)
Explanation: ***Pompe's disease*** - Also known as **glycogen storage disease type II**, it is caused by a deficiency of **acid alpha-glucosidase (GAA)**, a *lysosomal enzyme*. - This deficiency leads to the accumulation of **glycogen in lysosomes**, particularly affecting muscle tissue, thereby earning its classification as both a glycogen storage disease and a lysosomal storage disease. *Von Gierke's disease* - This is **glycogen storage disease type I** and is due to a deficiency in **glucose-6-phosphatase**. - It primarily affects the **liver and kidneys**, causing severe **hypoglycemia** and **lactic acidosis**, but it is not classified as a lysosomal storage disease. *McArdle's disease* - This is **glycogen storage disease type V**, caused by a deficiency in **muscle glycogen phosphorylase (myophosphorylase)**. - It manifests as **exercise intolerance** and muscle pain, but it does not involve lysosomal enzyme defects or glycogen accumulation in lysosomes. *Andersen's disease* - This is **glycogen storage disease type IV**, caused by a deficiency in the **glycogen branching enzyme**. - It leads to the formation of **abnormal glycogen structures**, primarily affecting the liver and causing early liver failure, but it is not a lysosomal storage disorder.
Question 766: Glucose is converted to glucuronate by which process?
- A. Oxidation of aldehyde group
- B. Oxidation of both
- C. Oxidation of the terminal alcohol group (Correct Answer)
- D. None of the options
Explanation: ***Oxidation of the terminal alcohol group*** - **Glucuronate** is formed by the **oxidation of the C-6 carbon** (the terminal primary alcohol group) of glucose. - This process is crucial for the detoxification of various substances in the body, as glucuronate is a key component in **glucuronidation reactions**. *Oxidation of aldehyde group* - Oxidation of the **aldehyde group (C-1)** of glucose typically forms **gluconic acid**, not glucuronate. - Gluconate is derived from the oxidation of the first carbon, while glucuronate is derived from the oxidation of the last carbon. *Oxidation of both* - If both the aldehyde group (C-1) and the terminal alcohol group (C-6) of glucose were oxidized, it would result in the formation of **glucaric acid** (saccharic acid), not glucuronate. - Glucaric acid has two carboxyl groups, one at each end of the molecule. *None of the options* - This option is incorrect because the specific biochemical pathway for glucuronate formation involves the oxidation of the terminal alcohol group. - The conversion of glucose to glucuronate is a well-established metabolic process.
Question 767: Which of the following substances does not inhibit glycolysis?
- A. Fluoride
- B. Arsenite
- C. Iodoacetate
- D. Fluoroacetate (Correct Answer)
Explanation: ***Fluoroacetate*** - **Fluoroacetate** is not a direct inhibitor of glycolysis. Instead, it is metabolized to **fluorocitrate**, which then acts as an inhibitor of **aconitase** in the **Krebs cycle (TCA cycle)**, thereby affecting cellular respiration at a later stage. - Its primary role in metabolic inhibition is within the **mitochondria**, impacting energy production via the TCA cycle rather than the glycolytic pathway. *Fluoride* - **Fluoride** is a known inhibitor of **enolase**, an enzyme in the penultimate step of glycolysis. - It forms a complex with **magnesium** and **phosphate** to block the active site of enolase, preventing the conversion of 2-phosphoglycerate to phosphoenolpyruvate. *Arsenite* - **Arsenite** inhibits glycolysis by targeting enzymes containing **sulfhydryl (–SH) groups**, particularly **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**, a critical enzyme in the glycolytic pathway. - It also inhibits the **pyruvate dehydrogenase complex** (linking glycolysis to the TCA cycle) and TCA cycle enzymes like **α-ketoglutarate dehydrogenase**, thereby affecting multiple stages of cellular respiration. *Iodoacetate* - **Iodoacetate** is a potent inhibitor of the enzyme **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**. - It specifically alkylates the **cysteine residue** at the active site of GAPDH, preventing the conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate, thereby blocking glycolysis.
Question 768: What cofactor is required for the proper functioning of glucose-6-phosphate dehydrogenase?
- A. NAD
- B. NADP (Correct Answer)
- C. FAD
- D. FMN
Explanation: ***NADP*** - **NADP+** (nicotinamide adenine dinucleotide phosphate) acts as the **electron acceptor** in the **glucose-6-phosphate dehydrogenase (G6PD)** reaction, becoming **NADPH**. - **NADPH** is crucial for maintaining the **redox balance** in cells, particularly in red blood cells, by reducing **oxidative stress**. *NAD* - **NAD+** (nicotinamide adenine dinucleotide) is a primary cofactor for many **dehydrogenase reactions** in catabolic pathways like **glycolysis** and the **Krebs cycle**. - It primarily functions as an electron acceptor in pathways that generate **ATP**, distinct from the role of **NADPH** in reductive biosynthesis and antioxidant defense. *FAD* - **FAD** (flavin adenine dinucleotide) is a coenzyme derived from **riboflavin (vitamin B2)** that is involved in various redox reactions, often in the form of **flavoproteins**. - Enzymes like **succinate dehydrogenase** in the electron transport chain utilize **FAD** as an electron acceptor, which is not the case for G6PD. *FMN* - **FMN** (flavin mononucleotide) is another coenzyme derived from **riboflavin**, structurally similar to FAD but lacking the additional adenosine monophosphate. - It participates in electron transfer reactions, particularly within **complex I** of the **electron transport chain**, but is not a cofactor for G6PD.
Question 769: Increased uric acid levels are seen in which glycogen storage disease ?
- A. Type I (Von Gierke's disease) (Correct Answer)
- B. Type II (Pompe disease)
- C. Type IV (Andersen disease)
- D. Type III (Cori disease)
Explanation: ***Type I (Von Gierke's disease)*** - In **Von Gierke's disease**, the deficiency of **glucose-6-phosphatase** leads to accumulation of glucose-6-phosphate in hepatocytes. - **Hyperuricemia** occurs due to: 1. **Increased purine degradation** - Metabolic stress leads to accelerated ATP breakdown and increased uric acid production 2. **Decreased renal excretion** - Lactic acidosis (from G6P → pyruvate → lactate) competitively inhibits uric acid secretion in renal tubules 3. **Enhanced purine synthesis** - Increased availability of ribose-5-phosphate from pentose phosphate pathway - Classic triad: **Hepatomegaly, hypoglycemia, and lactic acidosis with hyperuricemia** *Type II (Pompe disease)* - Caused by a deficiency of **acid alpha-glucosidase** (acid maltase), leading to glycogen accumulation in **lysosomes**. - Primarily affects the **heart**, **muscles**, and **liver**, but does not cause hyperuricemia. *Type IV (Andersen disease)* - Results from a deficiency of **glycogen branching enzyme**, leading to the formation of abnormal glycogen with long, unbranched chains. - Primarily affects the **liver** and **spleen**, causing cirrhosis and hepatic failure, but not hyperuricemia. *Type III (Cori disease)* - Caused by a deficiency of **glycogen debranching enzyme** (amylo-1,6-glucosidase), leading to abnormal accumulation of glycogen with short outer branches. - Presents with hepatomegaly, hypoglycemia, and muscle weakness, but **hyperuricemia is not a characteristic feature**.
Question 770: GLUT2 plays a functionally important role mainly in?
- A. Liver
- B. Pancreatic beta cells (Correct Answer)
- C. Skeletal muscle tissue
- D. Kidney
Explanation: ***Pancreatic beta cells*** - **GLUT2** acts as a **glucose sensor** in pancreatic beta cells, which is its **most functionally critical role** in the body. - Its high Km (~15-20 mM, low affinity) ensures that glucose uptake is **proportional to blood glucose concentration**, enabling the beta cells to accurately sense glucose levels and secrete insulin accordingly. - This glucose-sensing mechanism is **essential for maintaining glycemic homeostasis** and makes GLUT2's role in beta cells uniquely important compared to its presence in other tissues. - Without functional GLUT2 in beta cells, the body cannot properly regulate insulin secretion in response to changing glucose levels. *Liver* - While **GLUT2** is abundantly expressed in hepatocytes and allows for bidirectional glucose transport (both uptake and release), its role here is **facilitative rather than regulatory**. - The liver has multiple other glucose-regulating mechanisms (glucokinase, glucose-6-phosphatase, glycogen metabolism). - GLUT2's function in the liver is important but not as uniquely critical as its glucose-sensing role in beta cells. *Skeletal muscle tissue* - **Skeletal muscle** primarily utilizes **GLUT4** (not GLUT2) for insulin-dependent glucose uptake. - **GLUT2** is not significantly expressed in skeletal muscle tissue. - This makes GLUT2 functionally unimportant in skeletal muscle. *Kidney* - The **kidney** expresses **GLUT2** in proximal tubule cells where it participates in glucose reabsorption from the glomerular filtrate. - However, this role is **secondary to SGLT2** (sodium-glucose cotransporter 2), which performs the primary active reabsorption. - GLUT2's function here is important but not the **"mainly"** critical role compared to its glucose-sensing function in beta cells.
Practice by Chapter
Carbohydrate Chemistry and Classification
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Glycolysis: Reactions and Regulation
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Gluconeogenesis: Reactions and Regulation
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Glycogen Metabolism: Synthesis and Breakdown
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Glycogen Storage Diseases
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Pentose Phosphate Pathway
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Metabolism of Fructose and Galactose
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Disorders of Fructose and Galactose Metabolism
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Blood Glucose Regulation
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Diabetes Mellitus: Biochemical Aspects
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Glycosylation and Glycoproteins
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Lactose Intolerance and Galactosemia
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