Carbohydrate Metabolism Practice Questions

Q: GLUT3 is seen in

Neurons. ***Neurons*** - **GLUT3** is the primary glucose transporter in **neurons** and is responsible for maintaining a constant supply of glucose to the brain, even at low blood glucose concentrations. - Its high affinity for glucose ensures that brain cells can take up glucose efficiently, which is crucial for their high metabolic demands. *Pancreas* - The pancreas primarily uses **GLUT2** on its beta cells, which has a low affinity and high capacity for glucose, allowing it to sense high blood glucose levels. - **GLUT1** is also found in pancreatic alpha cells. *Liver* - The liver predominantly expresses **GLUT2**, which facilitates both **glucose uptake** and **release** depending on the metabolic state. - Its low affinity for glucose allows the liver to act as a glucose sensor and regulate blood glucose homeostasis. *Spleen* - While various immune cells within the spleen express glucose transporters, no single GLUT isoform, such as **GLUT3**, is uniquely or predominantly associated with the general function of the spleen. - Most cells in the spleen express **GLUT1**, which provides basal glucose uptake.

Q: Low insulin to glucagon ratio leads to increase in the activity of

Glucose-6-phosphatase. ***Glucose-6-phosphatase*** - A low **insulin to glucagon ratio** signals a state of **low blood glucose**, leading to increased **glucagon** secretion. - Glucagon activates **gluconeogenesis** and **glycogenolysis** in the liver, and **glucose-6-phosphatase** is a key enzyme in the final step of both pathways, releasing free glucose into the bloodstream. *Hexokinase* - This enzyme is responsible for the **phosphorylation of glucose in most tissues** to trap it within the cell for glycolysis. - Its activity is generally high during periods of **high glucose and insulin levels** to promote glucose utilization. *Glucokinase* - This is an isoform of hexokinase found in the **liver and pancreatic beta cells**, with a higher Km for glucose, meaning it is active primarily at **high glucose concentrations**. - Its activity is increased by **insulin**, promoting glucose uptake and utilization in times of plenty. *Pyruvate kinase* - This enzyme catalyzes the final step of **glycolysis**, converting phosphoenolpyruvate to pyruvate. - Its activity is stimulated by **insulin** and inhibited by **glucagon**, reflecting its role in glucose breakdown, not production.

Q: Glutathione is maintained in reduced state by the help of ?

HMP shunt. ***HMP shunt*** - The **hexose monophosphate (HMP) shunt** produces **NADPH**, which is crucial for reducing **oxidized glutathione** back to its reduced form via **glutathione reductase**. - **Reduced glutathione** protects cells from **oxidative damage** by detoxifying harmful **reactive oxygen species.** *Transamination* - **Transamination** is a process involving the transfer of an **amino group** from an amino acid to a keto acid. - This pathway is primarily involved in **amino acid metabolism** and the synthesis of **non-essential amino acids**, not directly in glutathione reduction. *Uronic acid pathway* - The **uronic acid pathway** is involved in the synthesis of **glycolipids**, **sugars**, and **vitamin C** (in some animals). - It does not directly produce **NADPH** or enzymes necessary for maintaining **glutathione** in its reduced state. *Glycogenesis* - **Glycogenesis** is the process of synthesizing **glycogen** from **glucose** for storage, typically occurring in the liver and muscles. - This pathway is involved in **glucose storage** and **energy regulation**, not in the **redox state of glutathione**.

Q: McArdle's disease is caused by deficiency of which enzyme?

Muscle phosphorylase. ***Muscle phosphorylase (Myophosphorylase)*** - McArdle's disease is **Glycogen Storage Disease Type V** caused by deficiency of **muscle phosphorylase** (myophosphorylase) - This enzyme is essential for **glycogenolysis in skeletal muscle**, breaking down glycogen to glucose-1-phosphate - Patients experience **exercise intolerance, muscle cramps, and myoglobinuria** after intense exercise - Characteristic **second-wind phenomenon** occurs when alternative energy sources (fatty acids, blood glucose) become available - Diagnosed by **ischemic forearm exercise test** showing no rise in venous lactate *Glucose-6-phosphatase* - Deficiency causes **Type I Glycogen Storage Disease (von Gierke disease)** - Affects **liver and kidneys**, not primarily skeletal muscle - Presents with **hepatomegaly, hypoglycemia, lactic acidosis** *Branching enzyme* - Deficiency causes **Type IV Glycogen Storage Disease (Andersen disease)** - Results in abnormal glycogen with **fewer branch points** - Presents with **progressive cirrhosis and hepatosplenomegaly** *Debranching enzyme* - Deficiency causes **Type III Glycogen Storage Disease (Cori disease)** - Affects both **liver and muscle** metabolism - Presents with **hepatomegaly, hypoglycemia, and mild myopathy**

Q: History of dislike for sweet food items is typically present in:

Hereditary fructose intolerance. ***Hereditary fructose intolerance*** - Patients with hereditary fructose intolerance develop severe symptoms like **nausea, vomiting, abdominal pain, and hypoglycemia** after ingesting fructose, leading to an aversive response and **dislike for sweet food items**. - This aversion is a protective mechanism, as avoiding fructose-containing foods (including many sweets) prevents the accumulation of toxic metabolites due to a deficiency in **hepatic aldolase B**. *Glycogen storage disease* - While glycogen storage diseases can cause hypoglycemia, they typically do not lead to a specific **aversion to sweet foods**. - The primary defect is in **glycogen synthesis or breakdown**, leading to symptoms like hepatomegaly, muscle weakness, and exercise intolerance. *Diabetes mellitus* - Patients with diabetes mellitus often have a **craving for sweet foods** due to uncontrolled blood glucose levels and insulin resistance, rather than a dislike. - The condition is characterized by **hyperglycemia** and may involve polydipsia, polyuria, and polyphagia. *Galactosemia* - Galactosemia involves an inability to metabolize galactose, leading to symptoms such as **vomiting, lethargy, and jaundice** upon milk ingestion [1]. - While patients will avoid milk, their aversion is not generally to all sweet foods, as sweet foods do not always contain galactose [1].

Q: All are Glucogenic hormones except?

ADH. ***ADH*** - **Antidiuretic hormone (ADH)** primarily regulates **water balance** by increasing water reabsorption in the kidneys, and does not directly promote glucose production. - While stress can increase ADH levels and indirectly affect glucose, ADH itself is not considered a primary **glucogenic hormone**. *Glucagon* - **Glucagon** is a key **glucogenic hormone** that raises blood glucose levels by stimulating **glycogenolysis** and **gluconeogenesis** in the liver. - It is released from pancreatic alpha cells in response to low blood glucose. *Glucocorticoids* - **Glucocorticoids** (e.g., cortisol) are potent **glucogenic hormones** that promote **gluconeogenesis** in the liver and reduce glucose utilization by peripheral tissues. - They help maintain blood glucose levels during stress and fasting. *Thyroxine* - **Thyroxine (T4)**, a thyroid hormone, increases **metabolic rate**, which includes enhancing glucose absorption from the gut, promoting **glycogenolysis**, and sometimes **gluconeogenesis**. - While not acting as directly on glucose as glucagon, it does contribute to **glucose homeostasis** through its metabolic effects.

Q: Which carbon of glucose is oxidized to form glucuronic acid?

Oxidation of the terminal alcohol group only. ***Oxidation of the terminal alcohol group only*** - Glucuronic acid is formed by the **oxidation of the C6 carbon (terminal alcohol group)** of glucose, while the aldehyde group (C1) remains intact. - This specific oxidation converts glucose into a **uronic acid**, essential for detoxification and connective tissue synthesis. *Oxidation of the aldehyde group only* - The oxidation of the **aldehyde group (C1)** of glucose would yield **gluconic acid**, not glucuronic acid. - This reaction typically occurs during the conversion of glucose to gluconolactone, a step in the pentose phosphate pathway for example. *No oxidation occurs* - The formation of glucuronic acid is explicitly an **oxidative process**, as a hydroxyl group is converted to a carboxyl group. - If no oxidation occurred, glucose would remain glucose, or undergo other non-oxidative transformations. *Oxidation of both the aldehyde and terminal alcohol groups* - Oxidation of **both the aldehyde (C1) and terminal alcohol (C6)** groups of glucose would lead to the formation of **glucaric acid (saccharic acid)**. - Glucaric acid has carboxyl groups at both ends, making it different from glucuronic acid, which only has a carboxyl group at C6.

Q: Glucagon acts on liver to cause:

Glycogenolysis. ***Glycogenolysis*** * **Glucagon's primary role** is to increase blood glucose levels during fasting states * Glucagon binds to **glucagon receptors on hepatocytes** (liver cells) * This activates **adenylyl cyclase → cAMP → protein kinase A** cascade * PKA phosphorylates and activates **phosphorylase kinase**, which activates **glycogen phosphorylase** * Result: **Glycogen breakdown to glucose-1-phosphate → glucose-6-phosphate → free glucose** (via glucose-6-phosphatase in liver) * The free glucose is released into bloodstream to maintain blood glucose levels *Kreb's cycle* * The **Kreb's cycle (citric acid cycle)** oxidizes acetyl-CoA to produce ATP, NADH, and FADH2 * It is not directly stimulated by glucagon; its activity is regulated by **substrate availability** and **energy demands** (ATP/ADP ratio, NADH/NAD+ ratio) * Glucagon's effects are primarily on glucose homeostasis, not directly on oxidative metabolism *Glycolysis* * **Glycolysis** breaks down glucose into pyruvate, generating ATP * Glucagon **inhibits glycolysis** in the liver by decreasing fructose-2,6-bisphosphate levels * This inhibition makes sense: glucagon's role is to **increase** blood glucose, not consume it * Glucagon activates phosphodiesterase which reduces cAMP levels needed for PFK-2 activity *Gluconeogenesis* * While glucagon does **stimulate gluconeogenesis** in the liver (glucose synthesis from non-carbohydrate sources) * The question asks about the direct action, and **glycogenolysis is the primary and immediate response** to glucagon * Gluconeogenesis is a slower process that becomes more important during prolonged fasting

Q: Which of the following is active in dephosphorylated state?

Glycogen Synthase. ***Glycogen Synthase*** - **Glycogen synthase** is primarily active in its **dephosphorylated state**, which is promoted by insulin and signals glycogen synthesis. - Dephosphorylation relieves the inhibitory effect of phosphorylation, allowing the enzyme to efficiently add glucose units to a **growing glycogen chain**. *PEPCK* - **Phosphoenolpyruvate carboxykinase (PEPCK)** activity is primarily regulated at the transcriptional level, not typically by phosphorylation state for activation. - Its expression is induced by **glucagon** and **cortisol** during gluconeogenesis. *Pyruvate Carboxylase* - **Pyruvate carboxylase** is allosterically activated by **acetyl-CoA** and its activity is not directly regulated by phosphorylation/dephosphorylation in the same manner as glycogen synthase. - This enzyme plays a key role in **gluconeogenesis** by converting pyruvate to oxaloacetate. *Glycogen Phosphorylase* - **Glycogen phosphorylase** is active in its **phosphorylated state**, particularly the 'a' form, which is promoted by glucagon and adrenaline for glycogen breakdown. - Phosphorylation activates the enzyme, leading to the **breakdown of glycogen** into glucose-1-phosphate.

Q: Which of the following is the PRIMARY physiological action of insulin in the fed state?

Activation of key enzymes of glycolysis. ***Activation of key enzymes of glycolysis*** - In the fed state, **insulin's primary and immediate action** is to promote **glucose utilization** through activation of glycolytic enzymes including **hexokinase, phosphofructokinase (PFK-1), and pyruvate kinase**. - This represents the **most direct and immediate metabolic response** to elevated blood glucose after a meal, allowing cells to use glucose for **immediate energy production**. - Insulin also promotes **GLUT4 translocation** to cell membranes in muscle and adipose tissue, enhancing glucose uptake, which directly feeds into **glycolysis**. - **Glycogen synthesis** (glycogenesis) occurs simultaneously as another primary action for glucose storage in liver and muscle. *Increased lipogenesis* - While insulin does stimulate **lipogenesis** (fatty acid and triglyceride synthesis) in the fed state, this is a **secondary action** that becomes significant primarily when **glycogen stores are replete**. - Lipogenesis represents **long-term energy storage**, but the primary immediate concern in the fed state is handling the glucose load through **direct utilization and glycogen storage**. - Only the excess glucose beyond immediate energy needs and glycogen storage capacity is converted to fat via lipogenesis. *Stimulation of gluconeogenesis* - This is **incorrect** - insulin **inhibits gluconeogenesis** in the fed state by suppressing key enzymes like **PEPCK and glucose-6-phosphatase**. - Stimulating gluconeogenesis would counteract insulin's primary function of **lowering blood glucose levels**. *Increased amino acid entry in the cell* - Insulin does promote **amino acid uptake** and **protein synthesis**, which is an important anabolic action. - However, in the context of the fed state's primary metabolic challenge (handling elevated blood glucose), **glucose utilization through glycolysis** takes precedence as the primary action.

Question 1

GLUT3 is seen in

Accepted Answer

Neurons

Answer

Pancreas

Answer

Liver

Answer

Spleen

Question 2

Low insulin to glucagon ratio leads to increase in the activity of

Accepted Answer

Glucose-6-phosphatase

Answer

Hexokinase

Answer

Glucokinase

Answer

Pyruvate kinase

Question 3

Glutathione is maintained in reduced state by the help of ?

Accepted Answer

HMP shunt

Answer

Transamination

Answer

Uronic acid pathway

Answer

Glycogenesis

Question 4

McArdle's disease is caused by deficiency of which enzyme?

Accepted Answer

Muscle phosphorylase

Answer

Glucose-6-phosphatase

Answer

Branching enzyme

Answer

Debranching enzyme

Question 5

History of dislike for sweet food items is typically present in:

Accepted Answer

Hereditary fructose intolerance

Answer

Glycogen storage disease

Answer

Diabetes mellitus

Answer

Galactosemia

Question 6

All are Glucogenic hormones except?

Accepted Answer

ADH

Answer

Glucagon

Answer

Glucocorticoids

Answer

Thyroxine

Question 7

Which carbon of glucose is oxidized to form glucuronic acid?

Accepted Answer

Oxidation of the terminal alcohol group only

Answer

Oxidation of the aldehyde group only

Answer

No oxidation occurs

Answer

Oxidation of both the aldehyde and terminal alcohol groups

Question 8

Glucagon acts on liver to cause:

Accepted Answer

Glycogenolysis

Answer

Kreb's cycle

Answer

Glycolysis

Answer

Gluconeogenesis

Question 9

Which of the following is active in dephosphorylated state?

Accepted Answer

Glycogen Synthase

Answer

PEPCK

Answer

Pyruvate Carboxylase

Answer

Glycogen Phosphorylase

Question 10

Which of the following is the PRIMARY physiological action of insulin in the fed state?

Accepted Answer

Activation of key enzymes of glycolysis

Answer

Stimulation of gluconeogenesis

Answer

Increased amino acid entry in the cell

Answer

Increased lipogenesis

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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