Blood Glucose Regulation — MCQs

10 questions

Which of the following statements correctly describes the effect of insulin and glucagon on gluconeogenesis?

A patient had dinner at 8 PM at night and does his blood sugar test at 7 AM in the morning. What is the major source of glucose at this time?

Which of the following statements best describes the mechanism of action of insulin on target cells?

An 8-month-old infant is brought in with poor feeding, lethargy, hypotonia, and hepatomegaly. Labs reveal hypoglycemia and metabolic acidosis. Which condition is most likely?

Which hormone is NOT increased in stress?

Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?

Insulin resistance down-regulates -

All of the following are increased in Acute stress except

Which of the following statements about insulin-mediated transport of glucose is correct?

Q10

Which one of the following statements concerning gluconeogenesis is correct?

Blood Glucose Regulation Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following statements correctly describes the effect of insulin and glucagon on gluconeogenesis?

A. Glucagon decreases fructose 2,6-bisphosphate levels, stimulating gluconeogenesis. (Correct Answer)
B. Insulin increases the levels of fructose 2,6-bisphosphate, which inhibits gluconeogenesis.
C. Insulin acts through a kinase to promote glycolysis.
D. Fructose 2,6-bisphosphate is an activator of glycolysis.

Explanation: ***Glucagon decreases fructose 2,6-bisphosphate levels, stimulating gluconeogenesis.*** - **Glucagon** activates **cAMP-dependent protein kinase (PKA)**, which phosphorylates the bifunctional enzyme **PFK-2/FBPase-2**. - Phosphorylation activates the **fructose-2,6-bisphosphatase (FBPase-2)** activity, which breaks down **fructose 2,6-bisphosphate (F-2,6-BP)**. - Decreased **F-2,6-BP** removes the inhibition of **fructose-1,6-bisphosphatase**, a key regulatory enzyme in gluconeogenesis, thereby **stimulating gluconeogenesis**. - This is the primary mechanism by which glucagon promotes glucose production during fasting states. *Insulin increases the levels of fructose 2,6-bisphosphate, which inhibits gluconeogenesis.* - While this statement is biochemically accurate, **insulin's primary role is to inhibit gluconeogenesis**, not stimulate it. - Insulin activates the **kinase activity (PFK-2)** of the bifunctional enzyme, increasing **F-2,6-BP** levels. - Elevated **F-2,6-BP** inhibits **fructose-1,6-bisphosphatase**, thereby inhibiting gluconeogenesis. - However, the question asks about effects on gluconeogenesis, and **glucagon's stimulatory effect is more directly relevant** to understanding gluconeogenesis regulation. *Fructose 2,6-bisphosphate is an activator of glycolysis.* - This statement is true but incomplete in the context of the question. - **F-2,6-BP** is a potent allosteric activator of **phosphofructokinase-1 (PFK-1)**, the rate-limiting enzyme of glycolysis. - However, this option doesn't directly address the hormonal regulation of **gluconeogenesis** as requested in the question stem. *Insulin acts through a kinase to promote glycolysis.* - While insulin does activate various kinases (e.g., **Akt/PKB**) that promote glycolysis, this statement is too vague. - The question specifically asks about effects on **gluconeogenesis**, not glycolysis. - Insulin's effect on gluconeogenesis is through inhibition (via increased F-2,6-BP levels), which is not clearly stated in this option.

Question 2: A patient had dinner at 8 PM at night and does his blood sugar test at 7 AM in the morning. What is the major source of glucose at this time?

A. Liver Glycogen (Correct Answer)
B. Muscle Glycogen
C. Gluconeogenesis
D. Dietary Carbohydrate
E. Ketone bodies

Explanation: ***Liver Glycogen*** - After an overnight fast (approximately 11 hours in this scenario), the primary mechanism for maintaining blood glucose levels is the breakdown of **liver glycogen** stores. - The liver is crucial for glucose homeostasis as it can release glucose directly into the bloodstream, a function muscle glycogen cannot perform. *Muscle Glycogen* - **Muscle glycogen** serves as an energy reserve primarily for the muscle itself and cannot be directly released into the bloodstream to maintain blood glucose levels. - It is utilized for physical activity and local energy demands within muscle cells. *Gluconeogenesis* - **Gluconeogenesis**, the synthesis of glucose from non-carbohydrate precursors, becomes increasingly important for glucose production after prolonged fasting (typically *after* liver glycogen stores are depleted). - While it contributes during an overnight fast, **liver glycogenolysis** is the dominant source initially. *Dietary Carbohydrate* - **Dietary carbohydrates** from the previous dinner (8 PM) would have been absorbed and utilized or stored as glycogen much earlier than 7 AM the next morning. - By 7 AM, the direct impact of the previous night's meal on circulating glucose is negligible, having been processed hours before. *Ketone Bodies* - **Ketone bodies** are alternative fuel sources produced during prolonged fasting or starvation, but they are **not glucose**. - While they can be used by tissues (brain, heart, muscle) for energy during extended fasting, they do not contribute to blood glucose levels and are metabolically distinct from glucose.

Question 3: Which of the following statements best describes the mechanism of action of insulin on target cells?

A. Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.
B. Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.
C. Insulin enters the cell and causes the release of calcium ions from intracellular stores.
D. Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor. (Correct Answer)

Explanation: ***Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.*** - **Insulin** is a **peptide hormone** and cannot freely pass through the lipid bilayer, thus it binds to a **transmembrane receptor** on the cell surface. - This binding leads to the activation of the receptor's intrinsic **tyrosine kinase activity** in the intracellular domain, initiating a signaling cascade. *Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.* - This mechanism describes the action of **steroid hormones**, which are lipid-soluble and can cross the cell membrane, binding to **intracellular receptors**. - **Insulin** acts via a **cell surface receptor** and its downstream effects are mediated through signal transduction pathways, not direct nuclear translocation. *Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.* - This mechanism is characteristic of **G-protein coupled receptors (GPCRs)**, which activate or inhibit enzymes like adenylate cyclase via G-proteins to produce second messengers like cyclic AMP. - The **insulin receptor** is a **receptor tyrosine kinase**, not a GPCR, and does not directly activate adenylate cyclase via Gs protein. *Insulin enters the cell and causes the release of calcium ions from intracellular stores.* - While some hormones and neurotransmitters can trigger the release of intracellular **calcium ions**, this is typically mediated by specific pathways (e.g., GPCRs linked to phospholipase C). - **Insulin** does not directly enter target cells to cause calcium release; its actions are primarily mediated through receptor tyrosine kinase signaling pathways.

Question 4: An 8-month-old infant is brought in with poor feeding, lethargy, hypotonia, and hepatomegaly. Labs reveal hypoglycemia and metabolic acidosis. Which condition is most likely?

A. Hereditary fructose intolerance
B. Galactosemia
C. Pompe disease
D. Von Gierke disease (Correct Answer)
E. Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency

Explanation: ***Von Gierke disease*** - **Type I glycogen storage disease** (GSD I) typically presents in infancy with **hypoglycemia** (due to impaired glucose release from glycogen), **hepatomegaly** (due to glycogen accumulation), and **lactic acidosis**. - Other common findings include **hyperlipidemia** and **hyperuricemia**, while **hypotonia** and **poor feeding** are generalized symptoms stemming from metabolic derangements. *Hereditary fructose intolerance* - This condition presents when **fructose** is introduced into the diet, typically after 4-6 months of age, with symptoms like **nausea, vomiting, abdominal pain**, and **hepatomegaly**. - While it can cause **hypoglycemia** and **metabolic acidosis**, the profound **hypotonia** and general metabolic collapse described in an 8-month-old on a typical diet makes GSD I more likely initially. *Galactosemia* - Symptoms usually appear within days or weeks of birth upon the initiation of **milk feeding**, including **vomiting, lethargy, poor feeding, jaundice, hepatomegaly**, and **cataracts**. - While it causes **hypoglycemia** and can lead to acidosis and hypotonia, the age of presentation and lack of specific mention of jaundice or cataracts makes it a less precise fit. *Pompe disease* - Also known as **glycogen storage disease type II**, it is characterized by the accumulation of glycogen in **lysosomes**, primarily affecting muscles. - The infantile form presents with severe **cardiomyopathy**, **muscle weakness**, and **hypotonia**, but **hypoglycemia** and **hepatomegaly** are not its primary or most prominent features. *Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency* - A **fatty acid oxidation disorder** that presents with episodic **hypoglycemia** (particularly during fasting or illness), **lethargy**, and **hepatomegaly**. - Key distinguishing features include **hypoketotic hypoglycemia** and elevated **dicarboxylic acids** on urine organic acids, but the **lactic acidosis** and overall metabolic profile are more consistent with GSD I.

Question 5: Which hormone is NOT increased in stress?

A. Glucagon
B. Insulin (Correct Answer)
C. Cortisol
D. Epinephrine

Explanation: ***Insulin*** - Insulin levels generally **decrease** during acute stress. This allows for increased availability of glucose for tissues, such as the brain and muscles, during "fight or flight" responses. - The sympathetic nervous system activity during stress **inhibits insulin secretion** from pancreatic beta cells. *Glucagon* - **Glucagon levels increase** during stress to promote **hepatic glucose production** (glycogenolysis and gluconeogenesis), ensuring a readily available energy supply. - This rise in glucagon is part of the counter-regulatory response to maintain blood glucose stability during stressful conditions. *Cortisol* - **Cortisol levels significantly increase** during stress as part of the **hypothalamic-pituitary-adrenal (HPA) axis** activation. - Cortisol mobilizes energy stores, suppresses the immune system, and prepares the body for prolonged stress. *Epinephrine* - **Epinephrine (adrenaline) levels increase rapidly** during acute stress as part of the **sympathetic nervous system** response. - It triggers the "fight or flight" response, increasing heart rate, blood pressure, and diverting blood flow to essential organs, while also promoting glucose release.

Question 6: Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?

A. Gluconeogenesis
B. TCA (Correct Answer)
C. HMP pathway
D. Glycolysis

Explanation: ***TCA (Tricarboxylic Acid Cycle)*** - The **TCA cycle** (also called Krebs cycle or citric acid cycle) is the **final common oxidative pathway** where all three macronutrients converge - **Carbohydrates** → Pyruvate → **Acetyl-CoA** (via pyruvate dehydrogenase) - **Lipids** → Fatty acids → **Acetyl-CoA** (via beta-oxidation) - **Proteins** → Amino acids → **Acetyl-CoA or TCA intermediates** (via deamination/transamination) - Complete oxidation of acetyl-CoA occurs in the TCA cycle, producing **NADH, FADH2, and GTP** for energy production *Gluconeogenesis* - This is a **biosynthetic pathway** that synthesizes glucose from non-carbohydrate precursors (lactate, glycerol, amino acids) - It is an **anabolic process**, not the catabolic final common pathway for energy production from all macronutrients *Glycolysis* - **Carbohydrate-specific pathway** that converts glucose to pyruvate - It is only the initial breakdown pathway for carbohydrates, not the common pathway where lipids and proteins also converge - Pyruvate from glycolysis must enter TCA cycle for complete oxidation *HMP pathway (Pentose Phosphate Pathway)* - Parallel pathway to glycolysis that generates **NADPH** (for biosynthesis and antioxidant defense) and **ribose-5-phosphate** (for nucleotide synthesis) - Processes only **glucose-6-phosphate** from carbohydrate metabolism - Not involved in lipid or protein metabolism integration

Question 7: Insulin resistance down-regulates -

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

Explanation: ***GLUT-4*** - **Insulin resistance** primarily affects cells that express **GLUT-4**, such as **adipocytes** and **skeletal muscle cells**. - In insulin-resistant states, the translocation of **GLUT-4 transporters** to the cell membrane in response to insulin is impaired, leading to **reduced glucose uptake**. *GLUT-2* - **GLUT-2** is primarily found in the **liver**, **pancreatic beta cells**, kidneys, and small intestine. - Its function is to transport glucose **bidirectionally** and is not regulated by insulin in the same manner as GLUT-4; thus, it is not directly down-regulated by insulin resistance. *GLUT-1* - **GLUT-1** is responsible for **basal glucose uptake** in most cells, including **erythrocytes** and cells of the blood-brain barrier. - Its expression is constitutive and largely **insulin-independent**, meaning it is not significantly down-regulated in insulin resistance. *GLUT-3* - **GLUT-3** is predominantly found in **neurons** and is crucial for **glucose transport into the brain**. - It has a high affinity for glucose and its expression is also largely **insulin-independent**, making it unaffected by insulin resistance in most contexts.

Question 8: All of the following are increased in Acute stress except

A. Growth hormone
B. Epinephrine
C. Glucagon
D. Insulin (Correct Answer)

Explanation: ***Insulin*** - During acute stress, **insulin secretion is actively suppressed** by catecholamines (epinephrine and norepinephrine) acting on **alpha-2 adrenergic receptors** on pancreatic beta cells. - This suppression is crucial for the stress response, as it allows **unopposed action of counter-regulatory hormones** to mobilize glucose and raise blood glucose levels. - The body prioritizes **immediate energy availability** (high blood glucose) over storage, making insulin the hormone that is **decreased, not increased**, during acute stress. *Growth hormone* - **Growth hormone** is a counter-regulatory hormone that **increases during acute stress** to mobilize energy stores, particularly by promoting lipolysis and gluconeogenesis. - Its actions contribute to the stress-induced elevation of **blood glucose levels**. *Epinephrine* - **Epinephrine** (adrenaline) is a primary catecholamine released during acute stress, leading to a rapid **fight or flight response**. - It significantly **increases heart rate**, blood pressure, and **glucose mobilization** through glycogenolysis and gluconeogenesis. *Glucagon* - **Glucagon** is a key hormone involved in **maintaining glucose homeostasis** and is significantly **increased during acute stress**. - It primarily acts on the liver to **stimulate glycogenolysis** and **gluconeogenesis**, thereby raising blood glucose levels to provide energy.

Question 9: Which of the following statements about insulin-mediated transport of glucose is correct?

A. Via GLUT-2
B. Main mechanism in RBCs
C. Seen in adipose tissue (Correct Answer)
D. Occurs primarily in the brain

Explanation: ***Seen in adipose tissue*** - **Adipose tissue** and **skeletal muscle** are the primary sites where glucose uptake from the bloodstream is significantly enhanced by insulin. - Insulin stimulates the translocation of **GLUT4 transporters** to the cell membrane in these tissues, increasing glucose entry. *Occurs primarily in the brain* - Glucose uptake into the **brain** is largely **insulin-independent**, primarily mediated by **GLUT1** and **GLUT3 transporters**. - The brain requires a constant supply of glucose and does not rely on insulin to facilitate its entry. *Via GLUT-2* - **GLUT2** is a **low-affinity, high-capacity** glucose transporter primarily found in the **liver**, **pancreatic beta cells**, kidneys, and small intestine. - It allows for rapid equilibration of glucose across membranes but is not directly involved in the **insulin-mediated uptake** seen in peripheral tissues. *Main mechanism in RBCs* - **Red blood cells (RBCs)** primarily use **GLUT1** for glucose transport, which is an **insulin-independent** process. - RBCs do not contain mitochondria and rely on glycolysis for energy, so they require a continuous, insulin-independent supply of glucose.

Question 10: Which one of the following statements concerning gluconeogenesis is correct?

A. It occurs primarily in the liver.
B. It is stimulated by elevated levels of acetyl CoA.
C. It is important in maintaining blood glucose during the normal overnight fast. (Correct Answer)
D. It is primarily inhibited by insulin.

Explanation: ***It is important in maintaining blood glucose during the normal overnight fast.*** - **This is the BEST answer** as it emphasizes the **primary physiological role** of gluconeogenesis in human metabolism. - During the **overnight fast** (8-12 hours), hepatic glycogen stores become depleted, making gluconeogenesis the **critical mechanism** to maintain blood glucose for glucose-dependent tissues like the **brain** (requires ~120g glucose/day) and **red blood cells**. - Without gluconeogenesis, blood glucose would drop dangerously during fasting, leading to hypoglycemia and neurological dysfunction. *It occurs primarily in the liver.* - This statement is **technically correct** - the liver accounts for approximately **90%** of total gluconeogenesis under normal conditions. - However, the **kidney cortex** also contributes significantly (10% normally, up to 40% during prolonged fasting), and the **intestine** plays a minor role. - While true, this is more of a **anatomical fact** rather than highlighting the critical physiological importance of the pathway, making it a less comprehensive answer than Option 1. *It is stimulated by elevated levels of acetyl CoA.* - This statement is **biochemically correct** - **Acetyl-CoA** is an important **allosteric activator** of **pyruvate carboxylase**, the first committed enzyme of gluconeogenesis. - However, this represents just **one regulatory mechanism** at the enzymatic level, not the overall physiological significance. - Primary regulation occurs through **hormones** (glucagon, cortisol, epinephrine) that coordinate the entire pathway, making this a narrower answer than Option 1. *It is primarily inhibited by insulin.* - This statement is also **correct** - **Insulin** is the primary hormonal **inhibitor** of gluconeogenesis. - Insulin suppresses gluconeogenesis by inhibiting key enzymes (PEPCK, glucose-6-phosphatase) and decreasing transcription of gluconeogenic genes. - However, this describes **inhibition** rather than the positive physiological role, making it less representative of gluconeogenesis's essential function than Option 1. **Note:** All four statements are technically correct, but Option 1 best captures the **essential physiological importance** of gluconeogenesis in human metabolism, which is why it is the preferred answer for this question.

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