Carbohydrate Metabolism Practice Questions

Q: At which step in glycolysis is NADH produced during the oxidation of glyceraldehyde-3-phosphate?

Glyceraldehyde-3-phosphate dehydrogenase. ***Glyceraldehyde-3-phosphate dehydrogenase*** - This enzyme catalyzes the oxidation and **phosphorylation** of glyceraldehyde-3-phosphate, producing **1,3-bisphosphoglycerate**. - During this reaction, **NAD+ is reduced to NADH**, which is a crucial step for energy production. *Pyruvate kinase* - This enzyme catalyzes the final step of glycolysis, transferring a phosphate group from **phosphoenolpyruvate** to ADP, forming ATP and pyruvate. - This step involves **substrate-level phosphorylation** for ATP production, not NADH. *Enolase* - This enzyme catalyzes the dehydration of **2-phosphoglycerate** to form **phosphoenolpyruvate (PEP)**. - This reaction involves the removal of a water molecule and does not produce NADH. *PFK-1* - **Phosphofructokinase-1 (PFK-1)** catalyzes the phosphorylation of fructose-6-phosphate to **fructose-1,6-bisphosphate**. - This is an ATP-consuming and a crucial regulatory step in glycolysis, but it does not involve NADH production.

Q: GLUT2 plays a functionally important role mainly in?

Pancreatic beta cells. ***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.

Q: Which carbohydrate is primarily metabolized by Aldolase-B?

Fructose. ***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.

Q: Which of the following metabolites is involved in glycogenolysis, glycolysis and gluconeogenesis ?

Glucose-6-phosphate. ***Glucose-6-phosphate*** - In **glycogenolysis**, **glycogen phosphorylase** breaks down glycogen into **glucose-1-phosphate**, which is then converted into **glucose-6-phosphate** by **phosphoglucomutase**. - In **glycolysis**, **glucose-6-phosphate** is isomerized to **fructose-6-phosphate** by **phosphoglucose isomerase**, committing it to the glycolytic pathway. - In **gluconeogenesis**, **glucose-6-phosphate** is the final product formed from other precursors; it can then be dephosphorylated to free glucose by **glucose-6-phosphatase**. *Galactose-1-phosphate* - This is an intermediate specifically in **galactose metabolism**, not directly involved in the central common pathways of glycogenolysis, glycolysis, or gluconeogenesis. - It is converted to **glucose-1-phosphate** via the **Leloir pathway** (involving **galactose-1-phosphate uridylyltransferase**), which can then enter glycogen metabolism. *Uridine diphosphoglucose* - **UDP-glucose** is crucial for **glycogen synthesis** (**glycogenesis**), serving as the activated glucose donor. - It is not directly a metabolite in the catabolic process of glycogenolysis, nor is it a direct intermediate in glycolysis or gluconeogenesis. *Fructose-6-phosphate* - **Fructose-6-phosphate** is a key intermediate in **glycolysis** and **gluconeogenesis**, specifically downstream from **glucose-6-phosphate**. - However, it is not directly produced from glycogenolysis; **glucose-6-phosphate** is the direct link between glycogenolysis and glycolysis.

Q: Increased uric acid levels are seen in which glycogen storage disease ?

Type I (Von Gierke's disease). ***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**.

Q: Which enzyme is active when the insulin:glucagon ratio is low?

Glucose-6-phosphatase. ***Glucose-6-phosphatase*** - A low **insulin:glucagon ratio** occurs during **fasting, starvation, or stress** (catabolic state). - In this metabolic state, **glucose-6-phosphatase** is **highly active** in the **liver** (and kidneys), catalyzing the final step of both **gluconeogenesis** and **glycogenolysis**. - It converts **glucose-6-phosphate** to **free glucose**, which is released into the bloodstream to maintain **blood glucose levels**. - This enzyme is stimulated by **glucagon** and inhibited by **insulin**. *Fructokinase* - This enzyme phosphorylates **fructose** to **fructose-1-phosphate** in the liver. - It is regulated by **fructose availability**, not by the **insulin:glucagon ratio**. - During a low insulin:glucagon state, **gluconeogenic** and **glycogenolytic** pathways are favored, not fructose metabolism. *Lactate dehydrogenase* - **LDH** interconverts **pyruvate** and **lactate** and functions in both **glycolysis** and **gluconeogenesis**. - While it plays a role in various metabolic states, it is **not specifically activated** by a low insulin:glucagon ratio. - It operates constitutively based on substrate availability rather than hormonal regulation. *Acetyl-CoA carboxylase* - This is the **rate-limiting enzyme** of **fatty acid synthesis** (lipogenesis). - It is **activated by insulin** (fed state) and **inhibited by glucagon** (fasted state). - When the insulin:glucagon ratio is **low**, this enzyme is **phosphorylated and INACTIVE**, shutting down fatty acid synthesis.

Q: Gluconeogenesis in the fasting state is indicated by:

Pyruvate Carboxylase activation by Acetyl CoA. ***Pyruvate Carboxylase activation by Acetyl CoA*** - In the **fasting state**, Acetyl CoA activates **pyruvate carboxylase**, shunting pyruvate away from glycolysis towards gluconeogenesis. - This activation is crucial for the synthesis of **oxaloacetate** from pyruvate, a key step in glucose production. *Citrate activation by acetyl-CoA carboxylase* - **Citrate** is an allosteric activator of **acetyl-CoA carboxylase**, which is involved in **fatty acid synthesis**, not gluconeogenesis. - This enzyme's activity is favored during states of **energy surplus**, not fasting. *Fructose 1,6 bisphosphate activates Pyruvate Kinase* - **Fructose 1,6-bisphosphate** activates **pyruvate kinase** as part of **glycolysis**, promoting glucose breakdown. - This regulatory mechanism operates during **fed states** to increase glucose utilization, which is opposite to the fasting state. *Fructose 2,6 bisphosphate activates PFK-1* - **Fructose 2,6-bisphosphate** activates **phosphofructokinase-1 (PFK-1)**, a key regulatory enzyme in **glycolysis**. - High levels of fructose 2,6-bisphosphate promote **glucose breakdown**, which is inhibited during the fasting state to conserve glucose.

Q: Which glycosaminoglycan is present in the cornea?

Keratan sulfate. ***Keratan sulfate*** - **Keratan sulfate** is a prominent **glycosaminoglycan (GAG)** found in the corneal stroma, playing a crucial role in maintaining corneal transparency. - Its unique structure and interaction with collagen fibrils contribute to the precise spacing and organization of the **corneal lamellae**. *Dermatan sulfate* - **Dermatan sulfate** is primarily found in the skin, blood vessels, and heart valves, but it is not a major GAG component of the cornea. - It is involved in regulating collagen fibril assembly and stability in these specific tissues. *Chondroitin sulfate* - **Chondroitin sulfate** is abundant in cartilage, bone, and connective tissues, providing resistance to compression. - While trace amounts might be present, it is not the primary GAG responsible for the unique properties of the cornea. *Hyaluronic acid* - **Hyaluronic acid**, a non-sulfated GAG, is found in the vitreous humor and synovial fluid, contributing to lubrication and hydration. - It is generally absent or present in very small quantities in the adult cornea under normal physiological conditions.

Q: Facilitative glucose transporters (GLUTs) comprise a large family. Which of the following is a glucose transporter in myocytes?

GLUT 4. ***GLUT 4*** - **GLUT 4** is the primary **insulin-dependent glucose transporter** found in **adipose tissue** and **striated muscle (skeletal and cardiac muscle)**, including myocytes. - Its translocation to the cell surface is stimulated by **insulin** and muscle contraction, facilitating glucose uptake into these cells. *GLUT 1* - **GLUT 1** is ubiquitously expressed in nearly all mammalian cells, providing a **basal level of glucose uptake**. - It is particularly abundant in **red blood cells** and the **blood-brain barrier**. *GLUT 2* - **GLUT 2** is a **low-affinity, high-capacity glucose transporter** found in the **liver, pancreatic beta cells, kidney, and small intestine**. - It plays a crucial role in **glucose sensing** and the release of insulin. *GLUT 3* - **GLUT 3** is primarily found in **neurons** and the **placenta**, where it is responsible for **high-affinity glucose uptake**. - It ensures a constant supply of glucose to these tissues, even at low blood glucose concentrations.

Question 1

At which step in glycolysis is NADH produced during the oxidation of glyceraldehyde-3-phosphate?

Accepted Answer

Glyceraldehyde-3-phosphate dehydrogenase

Answer

Pyruvate kinase

Answer

Enolase

Answer

PFK-1

Question 2

GLUT2 plays a functionally important role mainly in?

Accepted Answer

Pancreatic beta cells

Answer

Liver

Answer

Skeletal muscle tissue

Answer

Kidney

Question 3

Which carbohydrate is primarily metabolized by Aldolase-B?

Accepted Answer

Fructose

Answer

Galactose

Answer

Sucrose

Answer

None of the options

Question 4

Which of the following metabolites is involved in glycogenolysis, glycolysis and gluconeogenesis ?

Accepted Answer

Glucose-6-phosphate

Answer

Uridine diphosphoglucose

Answer

Fructose-6-phosphate

Answer

Galactose-1-phosphate

Question 5

Increased uric acid levels are seen in which glycogen storage disease ?

Accepted Answer

Type I (Von Gierke's disease)

Answer

Type II (Pompe disease)

Answer

Type IV (Andersen disease)

Answer

Type III (Cori disease)

Question 6

Which of the following statements BEST describes the net ATP production in glycolysis?

Accepted Answer

Glycolysis produces a net gain of 2 ATP per glucose molecule

Answer

Glycolysis produces 2 molecules of pyruvate

Answer

Hexokinase consumes ATP during glycolysis

Answer

Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules

Question 7

Which enzyme is active when the insulin:glucagon ratio is low?

Accepted Answer

Glucose-6-phosphatase

Answer

Fructokinase

Answer

Lactate dehydrogenase

Answer

Acetyl-CoA carboxylase

Question 8

Gluconeogenesis in the fasting state is indicated by:

Accepted Answer

Pyruvate Carboxylase activation by Acetyl CoA

Answer

Citrate activation by acetyl-CoA carboxylase

Answer

Fructose 1,6 bisphosphate activates Pyruvate Kinase

Answer

Fructose 2,6 bisphosphate activates PFK-1

Question 9

Which glycosaminoglycan is present in the cornea?

Accepted Answer

Keratan sulfate

Answer

Dermatan sulfate

Answer

Chondroitin sulfate

Answer

Hyaluronic acid

Question 10

Facilitative glucose transporters (GLUTs) comprise a large family. Which of the following is a glucose transporter in myocytes?

Accepted Answer

GLUT 4

Answer

GLUT 1

Answer

GLUT 2

Answer

GLUT 3

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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