Hormone Receptors and Signaling — MCQs
Insulin acts by which pathway-
Which of the following hormones does not mediate its action through cAMP?
Which of the following statements best describes the mechanism of action of insulin on target cells?
All these hormones primarily use cyclic adenosine monophosphate (cAMP) as their main second messenger pathway, except:
All the following mediate their action using cAMP as second messenger except:
Which of the following binds to intracellular receptors?
Regarding thyroid hormone all are true except:
What is the primary effect of GLP-1 on insulin secretion?
Secretion of prolactin is inhibited by?
Which of the following statements about G protein-coupled receptors (GPCRs) is true?
Hormone Receptors and Signaling Indian Medical PG Practice Questions and MCQs
Question 1: Insulin acts by which pathway-
- A. Tyrosine kinase (Correct Answer)
- B. Intrinsic ion channel
- C. JAK-STAT-Kinase
- D. Transcription factor
Explanation: ***Tyrosine kinase*** - Insulin binds to its receptor, a **receptor tyrosine kinase**, activating the intracellular tyrosine kinase domain. - This activation leads to the **autophosphorylation** of the receptor and subsequent phosphorylation of various intracellular substrates, initiating a signaling cascade. *Intrinsic ion channel* - This mechanism involves a receptor that is itself an **ion channel**, opening or closing to allow ions to pass through the cell membrane upon ligand binding. - Insulin's primary action is not to alter membrane permeability via direct ion channel modulation but rather to initiate an intracellular signaling cascade. *JAK-STAT-Kinase* - The **JAK-STAT pathway** is typically utilized by cytokine receptors (e.g., growth hormone, interleukins) that do not possess intrinsic kinase activity but activate associated soluble kinases like JAK. - Insulin signaling primarily utilizes its intrinsic tyrosine kinase activity rather than recruiting JAK kinases. *Transcription factor* - While insulin ultimately influences gene expression and thus the activity of **transcription factors**, it is not a transcription factor itself. - Insulin's initial binding and signaling occur at the cell surface via its receptor, leading to downstream events that *regulate* transcription factor activity.
Question 2: Which of the following hormones does not mediate its action through cAMP?
- A. Glucagon
- B. Follicle stimulating hormone
- C. Estrogen (Correct Answer)
- D. Luteinizing hormone
Explanation: ***Estrogen*** - **Estrogen** is a **steroid hormone** that mediates its action by binding to intracellular receptors, forming a complex that directly influences gene transcription. - Steroid hormones, due to their **lipophilicity**, can cross the cell membrane and do not typically rely on cell surface receptors or second messengers like cAMP. *Glucagon* - **Glucagon** acts on a **G protein-coupled receptor (GPCR)**, specifically a Gs-coupled receptor, leading to the activation of adenylyl cyclase. - This activation increases the intracellular concentration of **cAMP**, which then activates protein kinase A to mediate its effects, primarily on glucose metabolism. *Follicle stimulating hormone* - **FSH** binds to a **GPCR** on target cells, activating the Gs protein pathway. - This activation stimulates **adenylyl cyclase** and increases intracellular **cAMP** levels, which are critical for its role in gamete development. *Luteinizing hormone* - **LH**, like FSH, binds to a cell surface **GPCR** that activates the Gs protein. - This leads to the stimulation of **adenylyl cyclase** and an increase in **cAMP**, mediating its effects on steroidogenesis and ovulation.
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: All these hormones primarily use cyclic adenosine monophosphate (cAMP) as their main second messenger pathway, except:
- A. Dopamine (Correct Answer)
- B. Glucagon
- C. vasopressin
- D. Corticotropin
Explanation: ***Dopamine*** - **Dopamine** has dual signaling mechanisms depending on receptor subtype, making it unique among the listed hormones. - **D1-like receptors** (D1, D5) couple to Gs proteins and **increase cAMP** levels. - **D2-like receptors** (D2, D3, D4) couple to Gi proteins and **decrease/inhibit cAMP** production. - Since dopamine's effects are mediated through both cAMP-increasing and cAMP-decreasing pathways with significant physiological roles for both, it does **not primarily use cAMP** as a straightforward second messenger like the other hormones listed. - Therefore, dopamine is the exception as it has mixed cAMP signaling rather than primarily activating the cAMP pathway. *Corticotropin (ACTH)* - **Corticotropin** (ACTH) binds to melanocortin-2 receptors (MC2R) on the adrenal cortex and **primarily utilizes the cAMP pathway**. - Activation of adenylyl cyclase leads to increased intracellular cAMP, which activates protein kinase A (PKA). - This stimulates the synthesis and release of glucocorticoids (primarily cortisol). *Glucagon* - **Glucagon** binds to its G-protein coupled receptors on hepatocytes, leading to activation of adenylyl cyclase and increased intracellular **cAMP**. - The cAMP then activates protein kinase A, mediating glucagon's metabolic effects including **glycogenolysis and gluconeogenesis**. - This is a classic example of cAMP-mediated hormone action. *Vasopressin* - **Vasopressin** (ADH) primarily acts through **V2 receptors** in the renal collecting ducts, which use the **cAMP pathway** to increase water reabsorption (its primary physiological function). - V1 receptors (vasoconstriction) use the IP3/DAG pathway, but this is a secondary effect. - Since vasopressin's main clinical action is via cAMP-mediated V2 receptors, it primarily uses cAMP as its second messenger.
Question 5: All the following mediate their action using cAMP as second messenger except:
- A. Glucagon
- B. Dopamine
- C. Corticotropin
- D. Vasopressin (Correct Answer)
Explanation: ***Vasopressin (ADH)*** - Vasopressin has **dual signaling mechanisms** depending on receptor type: - **V2 receptors** (kidney collecting duct): Use **Gs-protein → cAMP pathway** for water reabsorption via aquaporin-2 insertion - **V1 receptors** (vascular smooth muscle): Use **Gq-protein → IP3/DAG pathway** for vasoconstriction - In the context of this question, vasopressin is considered the exception because it has **significant non-cAMP mediated actions** through V1 receptors, unlike the other hormones listed which **predominantly or exclusively** use cAMP - **Note**: This is a teaching point about receptor subtypes; vasopressin DOES use cAMP at V2 receptors *Glucagon* - **Exclusively uses cAMP pathway** in hepatocytes and adipocytes - Binds to **glucagon receptor** (GPCR) → **Gs-protein** → adenylyl cyclase activation → **increased cAMP** → PKA activation - Promotes glycogenolysis, gluconeogenesis, and lipolysis *Dopamine* - **D1 and D5 receptors** are **Gs-coupled** → **stimulate adenylyl cyclase** → **increase cAMP** - Important for neurotransmission (motor control, reward) and renal vasodilation - D2-family receptors (D2, D3, D4) inhibit cAMP but D1-family predominates in many physiological contexts *Corticotropin (ACTH)* - Binds to **melanocortin-2 receptor (MC2R)** on adrenal cortex - **Gs-protein coupled** → adenylyl cyclase activation → **increased cAMP** → PKA activation - Stimulates steroidogenesis and cortisol secretion - **Exclusively cAMP-dependent mechanism**
Question 6: Which of the following binds to intracellular receptors?
- A. Growth hormone
- B. Vitamin E
- C. Estrogen (Correct Answer)
- D. Insulin
Explanation: ***Estrogen*** - **Estrogen** is a **steroid hormone** that, due to its **lipophilic nature**, can easily pass through the cell membrane to bind to **intracellular receptors** in the cytoplasm or nucleus. - This binding leads to the formation of a **hormone-receptor complex** that acts as a transcription factor, regulating **gene expression**. *Growth hormone* - **Growth hormone** is a **peptide hormone** and therefore **hydrophilic**, meaning it cannot freely cross the cell membrane. - It binds to **transmembrane receptors** on the cell surface, initiating intracellular signaling cascades through pathways like the **JAK/STAT pathway**. *Vitamin E* - **Vitamin E** is a **lipid-soluble vitamin** and an important **antioxidant**, but it does not function as a signaling molecule that binds to intracellular receptors to regulate gene expression in the same manner as steroid hormones. - While it diffuses across membranes due to its lipophilicity, its primary role is to protect cell membranes from **oxidative damage**. *Insulin* - **Insulin** is a **protein hormone** that is **hydrophilic** and cannot pass through the cell membrane. - It binds to **tyrosine kinase receptors** on the cell surface, triggering a cascade of intracellular events like the **PI3K/Akt pathway** to regulate glucose metabolism.
Question 7: Regarding thyroid hormone all are true except:
- A. T4 has the maximum plasma concentration
- B. T3 is more avidly bound to nuclear receptors than T4
- C. T3 is more active than T4
- D. T4 has shorter half life than T3 (Correct Answer)
Explanation: ***T4 has shorter half-life than T3*** - This statement is incorrect because **T4 (thyroxine) has a significantly longer half-life (approximately 7 days)** compared to **T3 (triiodothyronine), which has a half-life of about 1-2 days**. - The longer half-life of T4 allows for a more stable and sustained effect, acting as a prohormone. *T4 has the maximum plasma concentration* - **T4 is secreted in much larger quantities from the thyroid gland than T3 (about 80% T4 vs. 20% T3)**, leading to a higher concentration in the plasma. - This high plasma concentration of T4 makes it the primary circulating thyroid hormone, mostly bound to plasma proteins. *T3 is more avidly bound to nuclear receptors than T4* - **T3 binds to nuclear thyroid hormone receptors with 10 to 15 times greater affinity than T4**, making it the more potent and biologically active form. - This stronger binding affinity is crucial for T3's direct physiological effects on target cells. *T3 is more active than T4* - **T3 is considered the metabolically active form of thyroid hormone**, directly mediating most physiological effects by binding to nuclear receptors. - T4 acts largely as a **prohormone**, being deiodinated in peripheral tissues to form T3, which then exerts metabolic activity.
Question 8: What is the primary effect of GLP-1 on insulin secretion?
- A. Increased aldosterone secretion by adrenal
- B. Increased PTH secretion
- C. Increased insulin secretion from beta-cells of pancreas (Correct Answer)
- D. Increased testosterone secretion from Leydig cells
Explanation: ***Increased insulin secretion from beta-cells of pancreas*** - **Glucagon-like peptide-1 (GLP-1)** is an **incretin hormone** that stimulates **glucose-dependent insulin secretion** from pancreatic beta-cells. - This effect is crucial for maintaining **glucose homeostasis**, especially after a meal. *Increased aldosterone secretion by adrenal* - **Aldosterone secretion** is primarily regulated by the **renin-angiotensin-aldosterone system (RAAS)** and potassium levels, not directly by GLP-1. - Aldosterone's main function is to regulate **sodium and water balance** and **blood pressure**. *Increased PTH secretion* - **Parathyroid hormone (PTH)** secretion is primarily regulated by **serum calcium levels**. - Its main role is to maintain **calcium homeostasis** by affecting bone, kidney, and intestine. *Increased testosterone secretion from Leydig cells* - **Testosterone secretion** from Leydig cells is primarily regulated by **luteinizing hormone (LH)** from the pituitary gland. - GLP-1 has no direct significant role in **gonadal steroidogenesis**.
Question 9: Secretion of prolactin is inhibited by?
- A. Dopamine (Correct Answer)
- B. Serotonin
- C. Noradrenaline
- D. Adrenaline
Explanation: ***Dopamine*** - **Dopamine**, produced by the **hypothalamus**, is the primary physiological inhibitor of **prolactin secretion** from the anterior pituitary gland. - It acts on **D2 receptors** on lactotrophs, leading to a decrease in prolactin synthesis and release. *Serotonin* - **Serotonin** generally has a stimulatory effect on **prolactin secretion**, rather than an inhibitory one. - Elevated serotonin levels can lead to **hyperprolactinemia**. *Noradrenaline* - While **noradrenaline** can have complex effects on pituitary hormones, it is not considered the primary direct inhibitor of **prolactin secretion**. - Its influence is often indirect or less potent than that of **dopamine**. *Adrenaline* - **Adrenaline** (epinephrine) is a neurotransmitter and hormone primarily involved in the **"fight or flight" response** and does not directly inhibit **prolactin secretion**. - Its effects on pituitary hormone release are typically less direct compared to **dopamine's** specific action on lactotrophs.
Question 10: Which of the following statements about G protein-coupled receptors (GPCRs) is true?
- A. The three subunits alpha, beta, and gamma must remain together as a complex for G protein to function.
- B. G proteins can act as either inhibitory or excitatory based on the type of alpha subunit. (Correct Answer)
- C. G proteins bind directly to hormones to become activated.
- D. In the resting state, G proteins are bound to GTP.
Explanation: ***G proteins can act as either inhibitory or excitatory based on the type of alpha subunit.*** - Different classes of Gα subunits (e.g., **Gαs**, **Gαi**, **Gαq**) couple to diverse downstream effectors, leading to either **stimulation** (excitatory) or **inhibition** of cellular processes. - For example, **Gαs** activates adenylyl cyclase, while **Gαi** inhibits it, demonstrating their opposing roles. *The three subunits alpha, beta, and gamma must remain together as a complex for G protein to function.* - Upon activation, the **Gα subunit dissociates** from the **Gβγ dimer**, and both free units can then independently modulate effector molecules. - For the G protein to function in signal transduction, the α subunit often separates from the βγ dimer to interact with its target enzyme or ion channel. *G proteins bind directly to hormones to become activated.* - **GPCRs** (the receptors themselves) bind to hormones or other ligands on the **extracellular side** of the membrane. - The binding of the ligand to the GPCR induces a conformational change in the receptor, which then activates the associated G protein on the intracellular side. *In the resting state, G proteins are bound to GTP.* - In the **resting (inactive) state**, the Gα subunit of the trimeric G protein is bound to **GDP**. - Activation occurs when the GPCR facilitates the exchange of **GDP for GTP** on the Gα subunit.
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