Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 711: Which among the following glucose transporters is present in beta cells?

A. GLUT1
B. GLUT2 (Correct Answer)
C. GLUT3
D. GLUT4

Explanation: ***GLUT2*** - **GLUT2** is a **low-affinity** glucose transporter predominantly found in pancreatic **beta cells**, liver, kidneys, and intestines. - Its low affinity allows beta cells to accurately sense high blood glucose levels, triggering **insulin release**. *GLUT1* - **GLUT1** is a widely distributed glucose transporter found in nearly all mammalian cells, including **red blood cells** and cells of the **blood-brain barrier**. - It exhibits **high affinity** for glucose, responsible for basal glucose uptake. *GLUT3* - **GLUT3** is a high-affinity glucose transporter primarily found in **neurons** and the **placenta**. - Its high affinity ensures a constant glucose supply to these metabolically demanding tissues, even at low blood glucose concentrations. *GLUT4* - **GLUT4** is an **insulin-sensitive** glucose transporter found in **adipose tissue** and **striated muscle** (skeletal and cardiac). - Its translocation to the cell surface from intracellular vesicles is stimulated by insulin, promoting glucose uptake into these tissues.

Question 712: Which of the following is NOT a key enzyme of gluconeogenesis?

A. Pyruvate carboxylase
B. PEP carboxykinase
C. Pyruvate kinase (Correct Answer)
D. Glucose-6-phosphatase

Explanation: ***Pyruvate kinase*** - **Pyruvate kinase** is a key regulatory enzyme in **glycolysis**, catalyzing the irreversible conversion of phosphoenolpyruvate (PEP) to pyruvate. - Since gluconeogenesis is essentially the reversal of glycolysis, pyruvate kinase is **NOT involved in gluconeogenesis**. Instead, this glycolytic step must be bypassed by different enzymes. - This is the correct answer as it is NOT a key enzyme of gluconeogenesis. *Pyruvate carboxylase* - This **IS a key enzyme of gluconeogenesis**, converting **pyruvate to oxaloacetate** in the mitochondria, thereby bypassing the pyruvate kinase step of glycolysis. - It uses **biotin** as a coenzyme and requires ATP. - This is one of the four key regulatory enzymes unique to gluconeogenesis. *PEP carboxykinase* - This **IS a key enzyme of gluconeogenesis**, converting **oxaloacetate to phosphoenolpyruvate (PEP)**, bypassing the irreversible pyruvate kinase step of glycolysis. - This enzyme is located in both the cytoplasm and mitochondria, depending on the species (cytoplasmic in humans). - This is one of the four key regulatory enzymes unique to gluconeogenesis. *Glucose-6-phosphatase* - This **IS a key enzyme of gluconeogenesis**, catalyzing the final step by dephosphorylating **glucose-6-phosphate to free glucose**, enabling its release from the liver into the bloodstream. - This enzyme bypasses the irreversible hexokinase/glucokinase step of glycolysis. - Located in the endoplasmic reticulum, it is exclusively found in gluconeogenic tissues like the liver and kidney.

Question 713: Neonatal hypoglycemia that does not respond to treatment with counter-regulatory hormones is diagnostic of which condition?

A. Von Gierke's disease (Correct Answer)
B. Hereditary fructose intolerance
C. Cori's disease (Glycogen storage disease type III)
D. Anderson's disease (Glycogen storage disease type IV)

Explanation: ***Von Gierke's disease*** - This condition (Glycogen Storage Disease Type I) results from a **deficiency of glucose-6-phosphatase**, essential for releasing glucose from the liver. - The inability to produce free glucose from glycogen or gluconeogenesis leads to severe hypoglycemia that **does not respond to counter-regulatory hormones** like glucagon, as the enzyme needed for glucose release is non-functional. *Hereditary fructose intolerance* - This condition involves a deficiency in **aldolase B**, leading to the accumulation of fructose-1-phosphate after fructose ingestion. - While it can cause hypoglycemia, it generally occurs after **fructose exposure** and is not characterized by hypoglycemia refractory to counter-regulatory hormones in the neonatal period without such exposure. *Cori's disease (Glycogen storage disease type III)* - Caused by a deficiency in the **glycogen debranching enzyme**, leading to the accumulation of abnormal glycogen. - Patients can present with hypoglycemia, but often respond to glucagon administration, as the remaining glycogen structure can still be partially broken down, unlike in Von Gierke's. *Anderson's disease (Glycogen storage disease type IV)* - Result of a deficiency in the **glycogen branching enzyme**, leading to the formation of abnormally structured glycogen with long, unbranched chains. - This disease primarily affects the liver and muscles, causing **cirrhosis** and muscle weakness, and typically does not present with severe, refractory neonatal hypoglycemia as the primary or most characteristic symptom.

Question 714: Which glucose transporter is primarily affected in diabetes mellitus?

A. GLUT-2
B. GLUT-5
C. GLUT-4 (Correct Answer)
D. SGLT-2

Explanation: ***GLUT-4*** - **GLUT-4** is the primary glucose transporter in **insulin-sensitive** tissues such as muscle and adipose tissue. - In **diabetes mellitus**, impaired insulin signaling leads to reduced translocation of GLUT-4 to the cell membrane, resulting in decreased glucose uptake by these tissues and subsequently **hyperglycemia**. *GLUT-2* - **GLUT-2** is found in the **liver**, **pancreatic beta cells**, kidneys, and small intestine. - It has a low affinity for glucose and is primarily involved in **high-capacity glucose transport**, serving as a glucose sensor in beta cells and allowing efficient glucose uptake/release in the liver. *GLUT-5* - **GLUT-5** is a fructose transporter predominantly found in the **small intestine** and testes. - It is responsible for the absorption of **fructose** from the diet and is not directly involved in glucose regulation relevant to diabetes mellitus. *SGLT-2* - **SGLT-2** (Sodium-Glucose Co-transporter 2) is found in the **proximal tubules of the kidneys**. - It is responsible for reabsorbing approximately 90% of the **filtered glucose** from the renal filtrate back into the bloodstream, and its inhibition is a therapeutic target in diabetes.

Question 715: Gas released from oligosaccharide metabolism by intestinal bacteria is

A. Carbon dioxide (Correct Answer)
B. Sulfur dioxide
C. Nitric oxide
D. Methane

Explanation: ***Carbon dioxide*** - **Carbon dioxide (CO₂)** is the **most universally produced gas** from oligosaccharide and carbohydrate fermentation by intestinal bacteria in the colon. - Nearly all colonic bacteria produce CO₂ during the fermentation of undigested carbohydrates and oligosaccharides. - Along with **hydrogen (H₂)**, CO₂ forms the bulk of intestinal gas from bacterial metabolism. - This is part of normal gut flora activity contributing to **flatulence**. *Methane* - While **methane (CH₄)** is produced during oligosaccharide fermentation, it is only generated by individuals harboring **methanogenic archaea** (approximately 30-50% of the population). - Methane production is not universal, unlike CO₂, making it less representative as "THE gas" from oligosaccharide metabolism. - Methanogens use H₂ and CO₂ to produce methane as a secondary process. *Sulfur dioxide* - **Sulfur dioxide (SO₂)** is primarily associated with industrial pollution and is not a product of normal intestinal bacterial metabolism. - Hydrogen sulfide (H₂S) may be produced from sulfur-containing compounds, but not sulfur dioxide. *Nitric oxide* - **Nitric oxide (NO)** is a signaling molecule involved in vasodilation and immune responses. - It is not a major gas produced from bacterial fermentation of oligosaccharides in the intestines.

Question 716: What is the biochemical structure of cellulose?

A. β (1,4) glucose (Correct Answer)
B. β (1,6) glucose
C. α (1,6) glucose
D. α (1,4) glucose

Explanation: ***β (1,4) glucose*** - Cellulose is a linear polysaccharide made of repeating **glucose units** joined by **β-1,4 glycosidic bonds**. - This specific linkage allows for strong hydrogen bonding between adjacent cellulose chains, contributing to its structural rigidity in plant cell walls. *α (1,4) glucose* - This linkage is characteristic of starch (amylose) and glycogen, forming helical structures that are readily digestible by humans. - Unlike cellulose, these **α-1,4 linkages** result in a coiled, rather than linear, polysaccharide structure. *β (1,6) glucose* - While beta linkages are present in some polysaccharides, the **β-1,6 linkage** is not the primary linkage for the main chain of cellulose. - This linkage is primarily found at branch points in certain complex carbohydrates. *α (1,6) glucose* - This linkage forms branch points in branched polysaccharides like amylopectin (a component of starch) and glycogen. - It allows for a more compact and easily accessible energy storage molecule, very different from the structural role of cellulose.

Question 717: In the oxidative phase of pentose phosphate pathway, NADPH is produced in?

A. Cytosol (Correct Answer)
B. Mitochondria
C. Ribosome
D. Peroxisomes

Explanation: ***Cytosol*** - The **oxidative phase** of the **pentose phosphate pathway (PPP)**, which produces **NADPH**, occurs exclusively in the **cytosol**. - Two key enzymes generate NADPH: **glucose-6-phosphate dehydrogenase (G6PD)** and **6-phosphogluconate dehydrogenase**. - **NADPH** is crucial for **reductive biosynthesis** (e.g., fatty acid synthesis, cholesterol synthesis) and for maintaining **redox balance** (e.g., reducing glutathione to protect against oxidative stress). *Mitochondria* - While mitochondria are central to **oxidative phosphorylation** and the **Krebs cycle**, they primarily produce **NADH** and **FADH2** for ATP generation. - The pentose phosphate pathway does not occur in mitochondria. *Ribosome* - **Ribosomes** are responsible for **protein synthesis** (translation) and are not involved in metabolic pathways or NADPH production. - They are cellular machinery for translation, not metabolic compartments. *Peroxisomes* - **Peroxisomes** are involved in **fatty acid β-oxidation** and **detoxification** of hydrogen peroxide. - While peroxisomes have some oxidative enzymes, they are not the site of the pentose phosphate pathway or its NADPH production.

Question 718: What is the cause of lactose intolerance?

A. Deficiency of Galactokinase
B. Deficiency of Uridyl transferase
C. Deficiency of Lactase (Correct Answer)
D. Deficiency of Enteropeptidase

Explanation: ***Deficiency of Lactase*** - Lactose intolerance results from the insufficient production of the enzyme **lactase**, which is responsible for breaking down **lactose** (a disaccharide found in milk and dairy products) into glucose and galactose. - When lactase is deficient, undigested lactose passes into the colon, where it is fermented by bacteria, leading to symptoms like **bloating**, **gas**, **diarrhea**, and **abdominal pain**. *Deficiency of Galactokinase* - A deficiency in **galactokinase** causes **Type II galactosemia**, a disorder involving the inability to metabolize galactose. - This condition primarily leads to **cataracts** and does not directly cause the digestive symptoms associated with lactose intolerance. *Deficiency of Uridyl transferase* - A deficiency in **uridyl transferase** causes **classic galactosemia (Type I)**, the most severe form of galactosemia. - This condition results in a buildup of toxic galactose metabolites, leading to **liver damage**, **renal failure**, and **developmental delay**, not lactose intolerance. *Deficiency of Enteropeptidase* - **Enteropeptidase** (also known as enterokinase) is an enzyme in the small intestine that activates trypsinogen to trypsin, which then activates other pancreatic proteases. - A deficiency leads to **protein malabsorption** and failure to thrive, not the fermentation of lactose by gut bacteria.

Question 719: Which of the following enzymes participates exclusively in glycolysis?

A. Phosphofructokinase
B. Glucose-6-phosphate dehydrogenase
C. Hexokinase
D. Pyruvate kinase (Correct Answer)

Explanation: ***Pyruvate kinase*** - This enzyme catalyzes the **final step of glycolysis**, irreversibly converting **phosphoenolpyruvate (PEP)** to pyruvate, producing ATP. - **Exclusively participates in glycolysis** - it has no role in any other metabolic pathway, making it the most definitive answer. - All tissue-specific isoforms (M1, M2, L, R) perform the same glycolysis-exclusive function. *Phosphofructokinase* - **Phosphofructokinase-1 (PFK-1)** catalyzes the committed step of glycolysis (Fructose-6-P → Fructose-1,6-BP) and is technically exclusive to the glycolytic pathway. - However, when the question refers to "phosphofructokinase" generically, it could include **PFK-2**, which produces fructose-2,6-bisphosphate (a regulatory molecule, not a glycolytic intermediate) and is part of the regulatory mechanism rather than the pathway itself. - **Pyruvate kinase is more unambiguously exclusive** to glycolysis as a metabolic enzyme. *Hexokinase* - While essential for the initial step of glycolysis, **hexokinase** phosphorylates multiple hexoses (glucose, mannose, fructose) and its product (G6P) can enter **multiple pathways**: glycolysis, pentose phosphate pathway, or glycogen synthesis. - **Not exclusive to glycolysis** - it serves as a branch point enzyme. *Glucose-6-phosphate dehydrogenase* - This enzyme is the rate-limiting step of the **pentose phosphate pathway (PPP)**, not glycolysis. - It catalyzes the oxidation of G6P to produce **NADPH** and ribose-5-phosphate for nucleotide synthesis, thereby diverting glucose-6-phosphate **away from glycolysis**.

Question 720: Which of the following is not a step in gluconeogenesis?

A. Conversion of pyruvate to acetyl-CoA (Correct Answer)
B. Conversion of glucose-6-phosphate to glucose
C. Conversion of oxaloacetate to phosphoenolpyruvate
D. Conversion of fructose-1,6-bisphosphate to fructose-6-phosphate

Explanation: ***Conversion of pyruvate to acetyl-CoA*** - This step is a key irreversible reaction catalyzed by the **pyruvate dehydrogenase complex** that commits pyruvate to oxidative metabolism via the **Krebs cycle** or to fatty acid synthesis. - It is **not a part of gluconeogenesis**, as acetyl-CoA cannot be converted back to pyruvate or glucose in mammals. - This reaction is irreversible and represents a point of no return for glucose synthesis. *Conversion of glucose-6-phosphate to glucose* - This is the **final step in gluconeogenesis**, catalyzed by **glucose-6-phosphatase** in the liver and kidney. - This enzyme allows free glucose to be released into the bloodstream. - It is an essential gluconeogenic step that bypasses the irreversible hexokinase/glucokinase reaction of glycolysis. *Conversion of oxaloacetate to phosphoenolpyruvate* - This is a **key bypass step in gluconeogenesis** that overcomes the irreversible pyruvate kinase reaction in glycolysis. - It is catalyzed by **phosphoenolpyruvate carboxykinase (PEPCK)** and requires GTP. - This is crucial for synthesizing glucose from non-carbohydrate precursors like amino acids and lactate. *Conversion of fructose-1,6-bisphosphate to fructose-6-phosphate* - This is an important **bypass step in gluconeogenesis**, catalyzed by **fructose-1,6-bisphosphatase**. - This irreversible reaction bypasses the phosphofructokinase-1 step of glycolysis. - It is one of the three key regulatory steps unique to gluconeogenesis.

Practice by Chapter

Carbohydrate Chemistry and Classification

Practice Questions

Glycolysis: Reactions and Regulation

Practice Questions

Gluconeogenesis: Reactions and Regulation

Practice Questions

Glycogen Metabolism: Synthesis and Breakdown

Practice Questions

Glycogen Storage Diseases

Practice Questions

Pentose Phosphate Pathway

Practice Questions

Metabolism of Fructose and Galactose

Practice Questions

Disorders of Fructose and Galactose Metabolism

Practice Questions

Blood Glucose Regulation

Practice Questions

Diabetes Mellitus: Biochemical Aspects

Practice Questions

Glycosylation and Glycoproteins

Practice Questions

Lactose Intolerance and Galactosemia

Practice Questions

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