Pancreatic Hormones and Glucose Metabolism Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Pancreatic Hormones and Glucose Metabolism. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 1: Increased insulin is characterized by all of the following, except:
- A. Hypoglycemia
- B. Enhanced fatty acid synthesis
- C. Increased Intracellular potassium
- D. Increased Glucagon secretion (Correct Answer)
Pancreatic Hormones and Glucose Metabolism Explanation: ***Increased Glucagon secretion***
- **Insulin** primarily functions to lower blood glucose, and its release is typically inhibited by factors that trigger **glucagon** secretion, which aims to raise blood glucose.
- Increased insulin would generally lead to **decreased glucagon secretion** as the body attempts to maintain glucose homeostasis.
*Increased Intracellular potassium*
- Insulin promotes the uptake of **potassium** into cells, particularly muscle and liver cells, by stimulating the **Na+/K+ ATPase pump**.
- This action helps to lower serum potassium levels and can be utilized therapeutically in cases of hyperkalemia.
*Hypoglycemia*
- **Insulin** is the primary hormone responsible for lowering blood glucose levels by promoting glucose uptake by cells and inhibiting hepatic glucose production.
- Excess insulin, whether endogenous or exogenous, can lead to **hypoglycemia** if glucose intake does not match insulin action.
*Enhanced fatty acid synthesis*
- **Insulin** is an anabolic hormone that promotes energy storage, including the conversion of excess glucose into **fatty acids** in the liver and adipose tissue.
- This process, known as lipogenesis, is a key mechanism by which insulin contributes to the storage of energy reserves.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 2: The diagnosis of diabetes mellitus is certain in which of the following situations?
- A. Abnormal oral glucose tolerance in a 24-yrs-old woman who has been dieting
- B. A serum glucose level >7.8 mmol/L in a woman in her twenty-fifth week of gestation after a 50-g oral glucose load
- C. Persistent asymptomatic glycosuria in a 30-yrs-old woman
- D. Successive fasting plasma glucose concentrations of 8, 9, and 8.5 mmol/L in an asymptomatic, otherwise healthy individual. (Correct Answer)
Pancreatic Hormones and Glucose Metabolism Explanation: ***Successive fasting plasma glucose concentrations of 8, 9, and 8.5 mmol/L in an asymptomatic, otherwise healthy individual.***
- A definitive diagnosis of **diabetes mellitus** requires two separate fasting plasma glucose (FPG) levels of **≥7.0 mmol/L** (126 mg/dL) or higher [1]. The given values (8, 9, 8.5 mmol/L) meet this criterion.
- Since the individual is **asymptomatic**, two abnormal tests are typically needed to confirm the diagnosis, which is satisfied by the successive elevated fasting glucose levels.
*Abnormal oral glucose tolerance in a 24-yrs-old woman who has been dieting*
- **Dieting** can affect glucose metabolism and potentially lead to an abnormal oral glucose tolerance test (OGTT) result that does not accurately reflect diabetes.
- A single abnormal OGTT in a dieting individual without confirmatory tests or symptoms is not sufficient for a definitive diagnosis of diabetes.
*A serum glucose level >7.8 mmol/L in a woman in her twenty-fifth week of gestation after a 50-g oral glucose load*
- A serum glucose level >7.8 mmol/L after a **50-g glucose challenge** is a positive screening test for **gestational diabetes mellitus**, but it is not diagnostic [2].
- A positive screening test requires further confirmation with a **100-g or 75-g oral glucose tolerance test** to diagnose gestational diabetes.
*Persistent asymptomatic glycosuria in a 30-yrs-old woman*
- **Glycosuria** (glucose in the urine) without hyperglycemia (elevated blood glucose) can be due to a low **renal threshold for glucose**, a benign condition called renal glycosuria.
- While it warrants investigation for diabetes, persistent asymptomatic glycosuria alone is **not diagnostic** of diabetes unless accompanied by elevated blood glucose levels.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG 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)
Pancreatic Hormones and Glucose Metabolism 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.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 4: Somatostatin is secreted by which type of cells in the pancreas?
- A. Gamma cells
- B. Delta cells (Correct Answer)
- C. Alpha cells
- D. Beta cells
Pancreatic Hormones and Glucose Metabolism Explanation: ***Delta cells***
- **Delta cells** (δ-cells) of the pancreatic islets are responsible for secreting **somatostatin**.
- Somatostatin acts as a paracrine inhibitor, regulating the secretion of other pancreatic hormones like insulin and glucagon.
*Gamma cells*
- The term "gamma cells" is not a standard classification for pancreatic islet cells.
- Pancreatic islet cells are typically categorized as alpha, beta, delta, and PP (pancreatic polypeptide) cells.
*Alpha cells*
- **Alpha cells** (α-cells) are responsible for secreting **glucagon**.
- Glucagon primarily acts to raise blood glucose levels.
*Beta cells*
- **Beta cells** (β-cells) are the most abundant pancreatic islet cells and produce **insulin**.
- Insulin is crucial for lowering blood glucose by promoting glucose uptake into cells.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 5: Which of the following compounds antagonizes the actions of insulin?
- A. Substance P
- B. Growth hormone (Correct Answer)
- C. Neuropeptide Y
- D. Vasoactive intestinal peptide
Pancreatic Hormones and Glucose Metabolism Explanation: ***Growth hormone***
- **Growth hormone (GH)** is a potent **anti-insulin hormone** that raises blood glucose by promoting **gluconeogenesis** and reducing glucose utilization by peripheral tissues.
- It decreases **insulin sensitivity** in target tissues like muscle and adipose tissue, often leading to a temporary state of **insulin resistance**.
*Substance P*
- **Substance P** is a **neuropeptide** involved in pain transmission and inflammation, and its primary actions do not directly involve glucose metabolism or insulin antagonism.
- While it can influence local metabolic processes, it does not exert systemic effects on insulin action.
*Neuropeptide Y*
- **Neuropeptide Y (NPY)** is a **neurotransmitter** primarily involved in stimulating appetite and reducing energy expenditure, playing a role in weight regulation.
- Although it affects metabolic balance, NPY does not directly antagonize insulin's actions on glucose uptake or utilization.
*Vasoactive intestinal peptide*
- **Vasoactive intestinal peptide (VIP)** is a **neurotransmitter** and hormone that primarily affects smooth muscle relaxation, exocrine and endocrine secretions, and local blood flow.
- It does not directly antagonize insulin's effects on glucose metabolism or directly impact insulin sensitivity in a significant way.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 6: Insulin-dependent glucose transport is through
- A. GLUT 2
- B. GLUT 1
- C. GLUT 3
- D. GLUT 4 (Correct Answer)
Pancreatic Hormones and Glucose Metabolism Explanation: ***GLUT 4***
- **GLUT 4** is the primary glucose transporter responsible for **insulin-dependent glucose uptake** in cells such as adipocytes and skeletal muscle cells.
- In the presence of insulin, **GLUT 4** translocates from intracellular vesicles to the cell membrane, increasing glucose uptake.
*GLUT 2*
- **GLUT 2** is a **low-affinity**, high-capacity glucose transporter found in the **liver**, pancreatic beta cells, and intestines.
- Its function is largely **insulin-independent**, primarily facilitating glucose sensing and uptake during hyperglycemia.
*GLUT 1*
- **GLUT 1** is ubiquitous and responsible for **basal glucose uptake** in most cells, including red blood cells and endothelial cells.
- It ensures a constant supply of glucose to cells regardless of insulin levels, making it **insulin-independent**.
*GLUT 3*
- **GLUT 3** is a **high-affinity** glucose transporter predominantly found in **neurons** and the placenta.
- This transporter is crucial for maintaining a constant supply of glucose to the brain and is **insulin-independent**.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 7: Low insulin to glucagon ratio leads to increase in the activity of
- A. Hexokinase
- B. Glucokinase
- C. Glucose-6-phosphatase (Correct Answer)
- D. Pyruvate kinase
Pancreatic Hormones and Glucose Metabolism Explanation: ***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.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG 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
Pancreatic Hormones and Glucose Metabolism 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**.
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 9: Which hormone does not play a significant role in utero growth?
- A. Growth hormone (Correct Answer)
- B. Thyroid hormone
- C. Cortisol
- D. Insulin
Pancreatic Hormones and Glucose Metabolism Explanation: ***Growth hormone***
- While essential for postnatal growth, **growth hormone (GH)** plays a minimal role in fetal growth.
- Fetal growth is primarily regulated by other factors like **insulin**, **insulin-like growth factors (IGFs)**, and adequate nutrient supply.
*Thyroid hormone*
- **Thyroid hormones** are critical for fetal neurological development and skeletal maturation.
- Deficiency in utero can lead to **cretinism**, characterized by severe developmental delays.
*Cortisol*
- **Cortisol** is important for the maturation of many fetal organs, particularly the **lungs** (surfactant production).
- It also aids in preparing the fetus for birth and adapting to extrauterine life.
*Insulin*
- **Insulin** is a key anabolic hormone in utero, promoting nutrient uptake and utilization for fetal growth.
- Fetal hyperinsulinemia (e.g., in maternal diabetes) can lead to **macrosomia** (large-for-gestational-age birth weight).
Pancreatic Hormones and Glucose Metabolism Indian Medical PG Question 10: Which of the following is an effect of GLP-1?
- A. Increased PTH secretion
- B. Increased insulin secretion from beta-cells of pancreas (Correct Answer)
- C. Increased aldosterone secretion by adrenal
- D. Increased testosterone secretion from Leydig cells
Pancreatic Hormones and Glucose Metabolism Explanation: ***Increased insulin secretion from beta-cells of pancreas***
- **Glucagon-like peptide-1 (GLP-1)** is an **incretin hormone** that plays a crucial role in glucose homeostasis by enhancing **glucose-dependent insulin secretion** from pancreatic beta cells.
- GLP-1 also **suppresses glucagon secretion**, slows gastric emptying, and promotes satiety, further contributing to blood glucose control.
*Increased PTH secretion*
- **Parathyroid hormone (PTH)** secretion is primarily regulated by **serum calcium levels**, with low calcium stimulating its release.
- GLP-1 has no direct significant effect on PTH secretion; their regulatory pathways are distinct.
*Increased aldosterone secretion by adrenal*
- **Aldosterone secretion** from the adrenal cortex is mainly controlled by the **renin-angiotensin-aldosterone system (RAAS)** and potassium levels.
- GLP-1 does not directly stimulate aldosterone release; its actions are primarily metabolic.
*Increased testosterone secretion from Leydig cells*
- **Testosterone secretion** by **Leydig cells** in the testes is regulated by **luteinizing hormone (LH)** from the pituitary gland.
- There is no known direct physiological link between GLP-1 and testosterone production.
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