Carbohydrate Metabolism Practice Questions

Q: Gluconeogenesis is inhibited by?

Insulin. ***Insulin*** - **Insulin** is a key hormone released in response to high blood glucose, promoting glucose uptake and storage, and **inhibiting hepatic glucose production** through gluconeogenesis and glycogenolysis. - It achieves this by decreasing the transcription and activity of key gluconeogenic enzymes like **phosphoenolpyruvate carboxykinase (PEPCK)** and **glucose-6-phosphatase**. *Cholecystokinin* - **Cholecystokinin (CCK)** is a gastrointestinal hormone primarily involved in digestion, stimulating bile release and pancreatic enzyme secretion. - It does not directly regulate gluconeogenesis; its main role is related to **fat and protein digestion**. *5-alpha reductase* - **5-alpha reductase** is an enzyme involved in steroid metabolism, converting testosterone to the more potent androgen, dihydrotestosterone (DHT). - This enzyme has no direct role in the regulation of **gluconeogenesis**. *Glucagon* - **Glucagon** is a hormone that has the opposite effect of insulin, stimulating gluconeogenesis and glycogenolysis to increase blood glucose levels during fasting or hypoglycemia. - Its primary action is to **promote** hepatic glucose output, not inhibit it.

Q: Most Common enzyme deficient in galactosemics:

Galactose-1-phosphate uridyl transferase/GALT. ***Galactose-1-phosphate uridyl transferase/GALT*** - **GALT deficiency** is the most common cause of **classic galactosemia** (Type I), a severe inherited metabolic disorder. - This enzyme is crucial for converting **galactose-1-phosphate** to **glucose-1-phosphate** in the main pathway of galactose metabolism. - Accounts for approximately **95%** of all galactosemia cases. *Galactosidase* - **Galactosidase** enzymes are involved in the hydrolysis of galactose-containing oligosaccharides or glycoconjugates but are not the primary enzymes deficient in classic galactosemia. - This enzyme is not part of the Leloir pathway of galactose metabolism, which is the pathway affected in galactosemia. *UDP galactose epimerase* - Deficiency of **UDP galactose epimerase** (GALE) causes a milder form of galactosemia (Type III), but it is much less common than GALT deficiency. - GALE is involved in the interconversion of UDP-galactose and UDP-glucose. - This is the rarest form of galactosemia. *Galactokinase* - **Galactokinase deficiency** (GALK) causes a different, milder form of galactosemia (Type II), characterized by **cataracts** as the primary symptom. - It prevents the initial phosphorylation of galactose to galactose-1-phosphate. - This accounts for less than 5% of galactosemia cases.

Q: Which is branching enzyme?

Amylo-1, 4-1, 6-transglycolase. ***Amylo-1, 4-1, 6-transglycolase*** - This enzyme is also known as **glycogen branching enzyme**. - It catalyzes the formation of **α-1,6-glycosidic bonds** by transferring a segment of four to six glucosyl residues from the non-reducing end of a growing glycogen chain to another chain. *Glycogen synthase* - This enzyme is responsible for the **elongation of glycogen chains** by forming **α-1,4-glycosidic bonds**. - It adds glucose units to the non-reducing end of a pre-existing glycogen primer. *Glycogen Phosphorylase* - This enzyme is involved in **glycogen degradation**. - It catalyzes the **phosphorolytic cleavage** of α-1,4-glycosidic bonds, releasing glucose-1-phosphate. *Glucose-6 phosphatase* - This enzyme is primarily found in the **liver** and kidneys and is crucial for **gluconeogenesis** and **glycogenolysis**. - It dephosphorylates glucose-6-phosphate to **free glucose**, allowing its release into the bloodstream.

Q: Low glycemic index food is:

Has slower absorption. ***Has slower absorption*** - **Low glycemic index (GI)** foods are digested and absorbed more slowly, leading to a gradual rise in blood glucose and insulin levels. - This characteristic is beneficial for managing **blood sugar** and providing sustained energy. *Easily digestible* - **Easily digestible** foods often have a **high glycemic index** because their carbohydrates are rapidly broken down and absorbed. - Low GI foods, by contrast, contain more complex carbohydrates and fiber, making them slower to digest. *Increase glycogen deposits* - While all carbohydrates are eventually converted to **glucose** and can contribute to **glycogen synthesis**, low GI foods do not uniquely or preferentially increase glycogen deposits compared to high GI foods. - Glycogen synthesis is primarily influenced by insulin levels and the total amount of carbohydrates consumed, irrespective of GI. *Increases plasma glucose* - All carbohydrate-containing foods will eventually increase **plasma glucose**, but low GI foods cause a **slower and smaller rise** in blood glucose compared to high GI foods. - They prevent the sharp spikes in blood sugar that are associated with high GI foods.

Q: When the insulin:glucagon ratio is decreased, which enzyme is active?

Glucose-6-phosphatase. ***Glucose-6-phosphatase*** - A decreased insulin:glucagon ratio indicates a **fasting state** or **catabolic state**, promoting glucose production and release rather than storage. - **Glucose-6-phosphatase** is the key enzyme that enables glucose release from the liver by removing the phosphate group from glucose-6-phosphate, producing free glucose that can exit hepatocytes. - This enzyme is active during both **gluconeogenesis** and **glycogenolysis** and is only present in liver, kidney, and intestinal cells. *Glucokinase* - **Glucokinase** is active in the **fed state** when insulin levels are high and the insulin:glucagon ratio is increased. - It phosphorylates glucose to trap it in hepatocytes for glycogen synthesis and metabolism, which is the opposite of what occurs during fasting. *Phosphofructokinase* - **Phosphofructokinase (PFK-1)** is the rate-limiting enzyme of **glycolysis**, active when glucose needs to be broken down for energy. - It is stimulated by high insulin:glucagon ratios and inhibited during fasting when gluconeogenesis (the reverse pathway) is active. *Hexokinase* - **Hexokinase** phosphorylates glucose in peripheral tissues for intracellular utilization. - During a low insulin:glucagon ratio, the priority is glucose **release** from the liver, not glucose **uptake** and phosphorylation in tissues.

Q: Iodine gives red color with:

Dextrin. ***Dextrin*** - **Dextrin** gives a characteristic **bright red to red-violet color** with iodine solution, which is the most distinctive "red" color among polysaccharides. - Dextrin is an intermediate product formed during **starch hydrolysis**, with a molecular structure between starch and simple sugars. - This color reaction is used as a **qualitative test** to identify dextrin and monitor starch breakdown during digestion. *Glycogen* - **Glycogen** produces a **red-brown to mahogany brown color** with iodine, which is more brown than red. - This brownish-red color is due to its **highly branched structure** with shorter chain lengths compared to starch. - While it has a reddish tinge, the predominant color is **brown**, making it distinct from the bright red of dextrin. *Starch* - **Starch** (particularly amylose) gives a distinctive **blue-black color** with iodine solution. - This occurs due to formation of a **starch-iodine complex** where iodine molecules fit into the helical structure of amylose. - Amylopectin (branched component) produces a **red-purple color**, but whole starch appears blue-black due to amylose dominance. *Inulin* - **Inulin**, a fructose polymer, shows **no color reaction** with iodine solution. - This absence of reaction is because inulin lacks the helical structure needed for iodine complex formation.

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: 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: All are actions of insulin except :

Gluconeogenesis. ***Gluconeogenesis*** - Insulin's primary role is to **lower blood glucose levels**, and it does so by suppressing processes that produce glucose, such as **gluconeogenesis**. - **Gluconeogenesis** is the synthesis of glucose from non-carbohydrate precursors, and insulin inhibits the key enzymes involved in this pathway. *Glycolysis* - Insulin **promotes glycolysis** by stimulating the activity of key glycolytic enzymes like **glucokinase** and **phosphofructokinase-1**. - This action helps to **increase glucose utilization** within cells, thereby reducing blood glucose levels. *Lipogenesis* - Insulin **promotes lipogenesis**, the synthesis of fatty acids and triglycerides, especially in the liver and adipose tissue. - This is a key mechanism for **storing excess energy** when glucose levels are high. *Glycogenesis* - Insulin **stimulates glycogenesis**, which is the synthesis of **glycogen** from glucose, primarily in the liver and muscle cells. - This process helps to **store excess glucose** for later use, thus lowering blood glucose.

Question 1

Gluconeogenesis is inhibited by?

Accepted Answer

Insulin

Answer

Cholecystokinin

Answer

5-alpha reductase

Answer

Glucagon

Question 2

Most Common enzyme deficient in galactosemics:

Accepted Answer

Galactose-1-phosphate uridyl transferase/GALT

Answer

Galactosidase

Answer

UDP galactose epimerase

Answer

Galactokinase

Question 3

Which is branching enzyme?

Accepted Answer

Amylo-1, 4-1, 6-transglycolase

Answer

Glycogen synthase

Answer

Glycogen Phosphorylase

Answer

Glucose-6 phosphatase

Question 4

Low glycemic index food is:

Accepted Answer

Has slower absorption

Answer

Easily digestible

Answer

Increase glycogen deposits

Answer

Increases plasma glucose

Question 5

When the insulin:glucagon ratio is decreased, which enzyme is active?

Accepted Answer

Glucose-6-phosphatase

Answer

Glucokinase

Answer

Phosphofructokinase

Answer

Hexokinase

Question 6

Iodine gives red color with:

Accepted Answer

Dextrin

Answer

Glycogen

Answer

Starch

Answer

Inulin

Question 7

GLUT3 is seen in

Accepted Answer

Neurons

Answer

Pancreas

Answer

Liver

Answer

Spleen

Question 8

All are Glucogenic hormones except?

Accepted Answer

ADH

Answer

Glucagon

Answer

Glucocorticoids

Answer

Thyroxine

Question 9

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 10

All are actions of insulin except :

Accepted Answer

Gluconeogenesis

Answer

Glycolysis

Answer

Lipogenesis

Answer

Glycogenesis

Carbohydrate Metabolism — MCQs

Carbohydrate Metabolism — MCQs

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