Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism Indian Medical PG Practice Questions and MCQs

Question 711: 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 712: All of the following are true about lactate utilization in the liver except -

A. Cori's cycle shifts the metabolic burden from muscle to liver
B. Cori's cycle can not be sustained indefinitely because it is energetically unfavourable
C. Cori's cycle is linked to glycogen synthesis in muscle
D. Total net number of ATP formed because of Cori's cycle is 4 (Correct Answer)

Explanation: ***Total net number of ATP formed because of cori's cycle is 4*** - This statement is incorrect. The **Cori cycle (lactic acid cycle)** is an energy-consuming process overall, as **6 ATP** molecules are consumed in the liver for gluconeogenesis to resynthesize glucose from lactate, while only a total of **2 ATP** are gained from glycolysis in the muscle. - The primary purpose of the Cori cycle is not net ATP production, but rather to shift the metabolic burden and regenerate glucose for tissues that rely on glycolysis (e.g., muscle, red blood cells). *Cori's cycle shifts the metabolic burden from muscle to liver* - This is true because **lactate produced in muscle** (during anaerobic conditions) is transported to the liver, where it is converted back to glucose. - The liver then bears the metabolic cost of **gluconeogenesis**, allowing the muscle to continue glycolysis and ATP production. *Cori's cycle can not be sustained indefinitely because it is energetically unfavourable* - This is true because the cycle involves a net consumption of ATP. **Six ATP equivalents** are used in gluconeogenesis in the liver to convert two molecules of lactate to one molecule of glucose. - In contrast, the glycolysis that produces the two lactate molecules in muscle yields only **two net ATP**. This energy deficit makes prolonged reliance on the Cori cycle unsustainable. *Cori's cycle is linked to glycogen synthesis in muscle* - This is true because the **glucose produced by the liver** via gluconeogenesis (from lactate) is released into the bloodstream. - This glucose can then be taken up by muscles and other tissues to **replenish glycogen stores** or be used for energy.

Question 713: 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 714: 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 715: In glycogen synthesis the active form of glucose used is-

A. Glucose 6 phosphate
B. UDP glucose (Correct Answer)
C. GTP glucose
D. Glucose 1 phosphate

Explanation: **UDP glucose** - **UDP-glucose** (uridine diphosphate glucose) is the activated form of glucose that donates glucose units for the elongation of the **glycogen chain** during glycogen synthesis. - The formation of UDP-glucose from **glucose-1-phosphate** and **UTP** (uridine triphosphate) is catalyzed by UDP-glucose pyrophosphorylase, making glucose-1-phosphate a precursor, not the active form. *Glucose 6 phosphate* - **Glucose 6-phosphate** is an important intermediate in glycolysis and gluconeogenesis, and it can be isomerized to glucose 1-phosphate, but it is not the direct substrate for glycogen synthase. - Its formation is the first committed step in glucose metabolism within the cell, trapping glucose inside. *Glucose I phosphate* - **Glucose 1-phosphate** is a precursor to UDP-glucose, formed from glucose 6-phosphate by **phosphoglucomutase**. - While essential for glycogen synthesis, it is not the directly active form that donates glucose to the glycogen chain itself. *GTP glucose* - **GTP glucose** is not a known active form of glucose involved in glycogen synthesis. - **GTP** (guanosine triphosphate) is primarily involved in other metabolic processes, such as protein synthesis and signal transduction.

Question 716: 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 717: Insulin resistance down-regulates the translocation of which glucose transporter to the cell membrane?

A. GLUT-1
B. GLUT-2
C. GLUT-3
D. GLUT-4 (Correct Answer)

Explanation: ***GLUT-4*** - **Insulin resistance** primarily affects cells that express **GLUT-4**, such as muscle and adipose tissue, by impairing its translocation from intracellular vesicles to the cell membrane. - This reduced translocation leads to decreased glucose uptake in response to insulin, a hallmark of **type 2 diabetes**. *GLUT-1* - **GLUT-1** is responsible for basal glucose uptake in nearly all cells, including **erythrocytes** and endothelial cells of the blood-brain barrier. - Its activity is largely **insulin-independent** and not significantly affected by insulin resistance in the same way as GLUT-4. *GLUT-2* - **GLUT-2** is found primarily in **pancreatic β-cells**, hepatocytes, renal tubular cells, and enterocytes. - It has a low affinity but high capacity for glucose transport, playing a key role in **glucose sensing** and facilitating glucose flux in and out of these cells, independent of insulin translocation. *GLUT-3* - **GLUT-3** is predominantly expressed in **neurons** and the placenta, where it facilitates high-affinity glucose uptake. - It is crucial for maintaining the brain's glucose supply and its activity is also **insulin-independent**.

Question 718: Which of the following enzymes do not catalyze an irreversible step in glycolysis?

A. Pyruvate kinase
B. Phosphofructokinase
C. Hexokinase
D. Phosphoglycerate kinase (Correct Answer)

Explanation: ***Phosphoglycerate kinase*** - This enzyme catalyzes the conversion of **1,3-bisphosphoglycerate** to **3-phosphoglycerate**, generating ATP. - This reaction is considered reversible because the free energy change is close to zero under physiological conditions, allowing for both forward (glycolysis) and reverse (gluconeogenesis) flux. *Hexokinase* - This enzyme catalyzes the **irreversible phosphorylation** of glucose to glucose-6-phosphate, trapping glucose within the cell. - It is one of the key regulatory enzymes in glycolysis, and its irreversibility ensures that glucose uptake and phosphorylation proceed in one direction. *Pyruvate kinase* - This enzyme catalyzes the final, **irreversible step** of glycolysis, converting phosphoenolpyruvate to pyruvate and generating ATP. - This reaction is a major control point for glycolysis due to its large negative free energy change. *Phosphofructokinase* - This enzyme catalyzes the **irreversible phosphorylation** of fructose-6-phosphate to fructose-1,6-bisphosphate. - It is considered the **rate-limiting step** and a primary control point in glycolysis, making it highly regulated and unidirectional.

Question 719: 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 720: In which of the following pathways is UDP glucose not utilized?

A. Uronic acid pathway
B. Glycogen synthesis
C. Galactose metabolism
D. HMP shunt (Correct Answer)

Explanation: ***HMP shunt*** - The **Hexose Monophosphate Shunt (HMP shunt)**, also known as the **pentose phosphate pathway**, primarily uses **glucose-6-phosphate** as its substrate. - Its main products are **NADPH** and **ribose-5-phosphate**, and it does not involve **UDP-glucose**. *Uronic acid pathway* - The **uronic acid pathway** converts **glucose** to **glucuronic acid**, **L-xylulose**, and **ascorbic acid (in some animals)**, utilizing **UDP-glucose** as an intermediate. - Specifically, **UDP-glucose dehydrogenase** oxidizes UDP-glucose to **UDP-glucuronate**. *Glycogen synthesis* - In **glycogen synthesis (glycogenesis)**, **UDP-glucose** is the direct precursor for adding glucose units to the growing **glycogen chain**. - The enzyme **glycogen synthase** catalyzes the transfer of glucose from UDP-glucose to the non-reducing end of glycogen. *Galactose metabolism* - In **galactose metabolism**, **UDP-glucose** plays a crucial role in the conversion of **galactose-1-phosphate** to **glucose-1-phosphate**. - This occurs via the enzyme **galactose-1-phosphate uridyltransferase**, which exchanges UDP from UDP-glucose with the phosphate from galactose-1-phosphate, forming **UDP-galactose** and **glucose-1-phosphate**.

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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