Metabolic Regulation: Hormonal Control Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Metabolic Regulation: Hormonal Control. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 1: Stress hyperglycemia occurs due to all except -
- A. Increased level of ACTH
- B. Decreased level of norepinephrine (Correct Answer)
- C. Insulin resistance
- D. Increased level of cortisol
Metabolic Regulation: Hormonal Control Explanation: ***Decreased level of norepinephrine***
- **Norepinephrine** is a **catecholamine** that generally **increases blood glucose** by stimulating **glycogenolysis** and **gluconeogenesis**.
- Therefore, a *decrease* in norepinephrine would *reduce* stress-induced hyperglycemia, making this the exception.
*Increased level of ACTH*
- **ACTH (Adrenocorticotropic Hormone)** stimulates the adrenal glands to release **cortisol**, which contributes significantly to stress hyperglycemia.
- Increased ACTH levels therefore *promote* hyperglycemia in stress.
*Insulin resistance*
- **Insulin resistance** is a common feature during stress, where target cells become less responsive to insulin's effects.
- This reduced insulin sensitivity leads to higher circulating glucose levels, contributing to hyperglycemia.
*Increased level of cortisol*
- **Cortisol** is a key **stress hormone** that promotes **gluconeogenesis** (production of glucose from non-carbohydrate sources) and **glycogenolysis** (breakdown of glycogen to glucose).
- Elevated cortisol levels directly lead to an increase in blood glucose, causing hyperglycemia.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 2: 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)
Metabolic Regulation: Hormonal Control 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.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 3: Agent that acts through tyrosine kinase receptor is
- A. Insulin (Correct Answer)
- B. MSH
- C. TSH
- D. TRH
Metabolic Regulation: Hormonal Control Explanation: ***Insulin***
- **Insulin** binds to its receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and the activation of intracellular signaling pathways.
- This activation is crucial for glucose uptake and metabolism by various cells in the body.
*MSH*
- **Melanocyte-stimulating hormone (MSH)** acts primarily through **G protein-coupled receptors**, specifically melanocortin receptors.
- These receptors activate adenylyl cyclase, leading to an increase in intracellular cAMP.
*TSH*
- **Thyroid-stimulating hormone (TSH)** also acts via a **G protein-coupled receptor** on thyroid follicular cells.
- Its binding stimulates adenylyl cyclase, increasing cAMP and thus thyroid hormone synthesis and release.
*TRH*
- **Thyrotropin-releasing hormone (TRH)** binds to **G protein-coupled receptors** on pituitary thyrotrophs.
- This interaction activates the phospholipase C pathway, leading to the release of TSH.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 4: Which of the following is not a peptide/protein -
- A. Growth hormone
- B. Glucocorticoids (Correct Answer)
- C. PTH
- D. Insulin
Metabolic Regulation: Hormonal Control Explanation: ***Glucocorticoids***
- **Glucocorticoids** are **steroid hormones** derived from cholesterol, making them **lipids**, not peptides or proteins.
- They exert their effects by binding to **intracellular receptors** to regulate gene expression.
*Growth hormone*
- **Growth hormone (GH)** is a **peptide hormone** produced by the anterior pituitary gland.
- It plays a crucial role in **growth**, cell reproduction, and metabolism.
*PTH*
- **Parathyroid hormone (PTH)** is a **peptide hormone** secreted by the parathyroid glands.
- It primarily regulates **calcium** and phosphate levels in the blood.
*Insulin*
- **Insulin** is a **peptide hormone** produced by the beta cells of the pancreatic islets.
- Its main function is to regulate **glucose metabolism** by facilitating glucose uptake into cells.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 5: Which of the following is called hunger hormone?
- A. Ghrelin (Correct Answer)
- B. Insulin
- C. Leptin
- D. Cortisol
Metabolic Regulation: Hormonal Control Explanation: ***Ghrelin***
- **Ghrelin** is often referred to as the **"hunger hormone"** because it stimulates appetite, increases food intake, and promotes fat storage.
- It is primarily produced in the **stomach** and its levels rise before meals and decrease after meals.
*Insulin*
- **Insulin** is a hormone primarily involved in regulating **blood glucose levels** by facilitating glucose uptake into cells.
- It does not directly induce hunger but rather signals satiety and energy storage.
*Leptin*
- **Leptin** is known as the **"satiety hormone"** because it suppresses appetite and signals to the brain that the body has sufficient energy stores.
- It is produced by **adipose tissue** (fat cells) and helps regulate long-term energy balance.
*Cortisol*
- **Cortisol** is a **stress hormone** involved in the body's 'fight or flight' response, influencing metabolism, immune function, and inflammation.
- While chronic stress and elevated cortisol can indirectly affect appetite and food cravings, it is not primarily known as a hunger or satiety hormone.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 6: All the following hormones have receptors on the plasma membrane of target tissues except:
- A. Epinephrine
- B. Glucagon
- C. Estradiol (Correct Answer)
- D. Thyrotropin
Metabolic Regulation: Hormonal Control Explanation: ***Estradiol***
- **Estradiol** is a **steroid hormone** derived from cholesterol, making it **lipid-soluble**.
- Due to its lipid solubility, estradiol can readily pass through the **plasma membrane** and bind to **intracellular receptors** in the cytoplasm or nucleus.
*Epinephrine*
- **Epinephrine** is a **catecholamine hormone** and is **water-soluble**.
- Water-soluble hormones cannot cross the lipid bilayer of the plasma membrane and thus bind to **receptors located on the cell surface**.
*Glucagon*
- **Glucagon** is a **peptide hormone** and is **water-soluble**.
- Like other peptide hormones, it binds to **specific receptors embedded in the plasma membrane** to elicit its cellular effects via second messenger systems.
*Thyrotropin*
- **Thyrotropin**, also known as **Thyroid-Stimulating Hormone (TSH)**, is a **glycoprotein hormone** and is **water-soluble**.
- TSH exerts its action by binding to **receptors on the plasma membrane** of thyroid follicular cells.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 7: Which hormone is NOT increased in stress?
- A. Glucagon
- B. Insulin (Correct Answer)
- C. Cortisol
- D. Epinephrine
Metabolic Regulation: Hormonal Control 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.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 8: Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?
- A. Gluconeogenesis
- B. TCA (Correct Answer)
- C. HMP pathway
- D. Glycolysis
Metabolic Regulation: Hormonal Control 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
Metabolic Regulation: Hormonal Control Indian Medical PG Question 9: All of the following are increased in Acute stress except
- A. Growth hormone
- B. Epinephrine
- C. Glucagon
- D. Insulin (Correct Answer)
Metabolic Regulation: Hormonal Control 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.
Metabolic Regulation: Hormonal Control Indian Medical PG Question 10: All of these cause hyperglycemia except:
- A. Catecholamines
- B. Insulin (Correct Answer)
- C. Cortisol
- D. GH
Metabolic Regulation: Hormonal Control Explanation: ***Insulin***
- Insulin's primary function is to **lower blood glucose levels** by facilitating glucose uptake into cells and promoting glycogen synthesis.
- It counters the effects of hormones that elevate blood sugar, directly leading to a **decrease in hyperglycemia**.
*Catecholamines*
- **Catecholamines** (e.g., epinephrine, norepinephrine) increase blood glucose by promoting **glycogenolysis** and **gluconeogenesis**.
- They also **inhibit insulin secretion**, further contributing to elevated blood sugar.
*Cortisol*
- **Cortisol** is a **glucocorticoid** that raises blood glucose by increasing **gluconeogenesis** and reducing peripheral **glucose utilization**.
- It can also decrease insulin sensitivity, leading to **hyperglycemia**.
*GH*
- **Growth hormone (GH)** can induce **insulin resistance** in peripheral tissues, which leads to reduced glucose uptake.
- It also promotes **gluconeogenesis**, both contributing to elevated blood glucose levels.
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