Biochemistry
3 questionsWhich enzyme is primarily responsible for the fat metabolism in adipose tissue?
Which amino acid requires ascorbic acid for its formation in the body?
In the electron transport chain (ETC), which enzyme does cyanide inhibit?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 181: Which enzyme is primarily responsible for the fat metabolism in adipose tissue?
- A. Lipoprotein lipase
- B. Hormone-sensitive lipase (Correct Answer)
- C. Acid lipase
- D. Acid maltase
Explanation: ***Hormone-sensitive lipase*** - This enzyme is crucial for the **mobilization of stored triglycerides** in adipose tissue by hydrolyzing them into fatty acids and glycerol. - Its activity is stimulated by hormones like **epinephrine** and **norepinephrine** and inhibited by insulin, reflecting its role in regulating fat release during energy demand. *Lipoprotein lipase* - This enzyme is primarily located on the **endothelial surface of capillaries** in various tissues, including adipose tissue, muscle, and heart. - Its main role is to clear **triglyceride-rich lipoproteins** like chylomicrons and VLDL from the bloodstream, facilitating the uptake of fatty acids into cells for storage or energy, rather than direct fat metabolism within the adipose cell. *Acid lipase* - **Lysosomal acid lipase** functions within lysosomes to break down cholesterol esters and triglycerides that are taken up by cells. - Its primary role is in the degradation of lipids within the **lysosomal compartments**, not in the primary process of fat mobilization from adipose tissue stores. *Acid maltase* - Also known as **alpha-glucosidase**, this enzyme is a lysosomal enzyme responsible for breaking down glycogen into glucose. - Its function is related to **glycogen metabolism** and has no direct role in fat metabolism in adipose tissue.
Question 182: Which amino acid requires ascorbic acid for its formation in the body?
- A. Lysine
- B. Hydroxyproline (Correct Answer)
- C. Cysteine
- D. Proline
Explanation: ***Hydroxyproline*** - **Ascorbic acid (Vitamin C)** is an essential cofactor for **prolyl hydroxylase** and **lysyl hydroxylase** enzymes - These enzymes catalyze the **post-translational hydroxylation** of proline and lysine residues within collagen chains to form hydroxyproline and hydroxylysine - This hydroxylation is crucial for **stabilization of the collagen triple helix** structure - Hydroxyproline is formed by **modification of proline after incorporation into collagen**, not as a free amino acid - **Scurvy** (Vitamin C deficiency) results in defective collagen due to inadequate hydroxyproline formation *Lysine* - Lysine is an **essential amino acid** obtained from diet - Does not require ascorbic acid for its synthesis or formation - While lysine residues in collagen can be hydroxylated (forming hydroxylysine), the question asks about the amino acid whose formation requires Vitamin C *Cysteine* - Cysteine is a **sulfur-containing amino acid** synthesized from methionine via transsulfuration pathway - Its synthesis does not involve ascorbic acid *Proline* - Proline is a **non-essential amino acid** synthesized from glutamate - **Proline synthesis does not require ascorbic acid** - Proline serves as the precursor that gets hydroxylated to hydroxyproline within collagen
Question 183: In the electron transport chain (ETC), which enzyme does cyanide inhibit?
- A. Complex II (Succinate dehydrogenase)
- B. Cytochrome c oxidase (Complex IV) (Correct Answer)
- C. Complex I (NADH dehydrogenase)
- D. Complex III (Cytochrome bc1 complex)
Explanation: ***Cytochrome c oxidase (Complex IV)*** - Cyanide binds to the **ferric iron (Fe3+)** in the heme a3 component of cytochrome c oxidase, blocking the final transfer of electrons to oxygen. - This inhibition effectively halts the entire **electron transport chain** and **oxidative phosphorylation**, leading to rapid cellular energy depletion. *Complex I (NADH dehydrogenase)* - While other toxins can inhibit Complex I (e.g., rotenone, amytal), **cyanide specifically targets Complex IV**. - Inhibition here prevents the entry of electrons from **NADH** into the ETC, but it's not cyanide's primary site of action. *Complex III (Cytochrome bc1 complex)* - Complex III is involved in transferring electrons from **ubiquinol** to cytochrome c, but it is not directly inhibited by cyanide. - Antimycin A is a well-known inhibitor of Complex III. *Complex II (Succinate dehydrogenase)* - Complex II directly receives electrons from **succinate** in the citric acid cycle and passes them to ubiquinone, bypassing Complex I. - Cyanide does not inhibit Complex II; inhibitors of this complex include malonate.
Physiology
7 questionsThe primary site of vasopressin synthesis is
Wolff–Chaikoff effect is due to?
What is the normal range for the CSF/plasma glucose ratio?
Gas exchange in tissues takes place at?
Transducin is a protein found in:
Substance that is completely reabsorbed from the kidney?
During moderate exercise, the respiratory rate increases in response to which of the following?
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 181: The primary site of vasopressin synthesis is
- A. Supraoptic nucleus (Correct Answer)
- B. Preoptic nucleus
- C. Paraventricular nucleus
- D. Posterior pituitary
Explanation: ***Supraoptic nucleus*** - The **supraoptic nucleus** of the hypothalamus is the **primary site** for the synthesis of **vasopressin** (also known as antidiuretic hormone or ADH). - Approximately **80% of vasopressin** is produced by the neurosecretory cells in this nucleus. - The synthesized vasopressin is transported down axons to the posterior pituitary for storage and release. *Preoptic nucleus* - The **preoptic nucleus** is involved in various homeostatic functions, including **thermoregulation** and **sleep regulation**, but not the synthesis of vasopressin. - While it has neuronal connections to the hypothalamus, it does not produce ADH. *Paraventricular nucleus* - The **paraventricular nucleus** also synthesizes **both vasopressin and oxytocin**, accounting for approximately **20% of vasopressin production**. - While it does produce vasopressin, the **supraoptic nucleus remains the primary site**, making it the correct answer to this question. - The PVN also plays important roles in stress response and various autonomic functions. *Posterior pituitary* - The **posterior pituitary** (neurohypophysis) is responsible for the **storage and release** of vasopressin and oxytocin, not their synthesis. - These hormones are produced in the hypothalamic nuclei (supraoptic and paraventricular) and then transported down axonal tracts to the posterior pituitary.
Question 182: Wolff–Chaikoff effect is due to?
- A. Decreased iodination of MIT
- B. Excess iodine intake (Correct Answer)
- C. Suppression of TSH secretion
- D. Decreased conversion of T4 to T3
Explanation: ***Excess iodine intake*** - The **Wolff-Chaikoff effect** is a phenomenon where a high intake of iodine acutely **inhibits thyroid hormone synthesis** and release. - This effect protects the body from excessive thyroid hormone production during periods of very high iodine availability. *Decreased iodination of MIT* - While the Wolff-Chaikoff effect does inhibit **iodination**, the direct cause is the excessive iodine itself, which triggers an autoregulatory shutdown. - Decreased iodination is a *consequence* of the high iodine leading to inhibition of thyroid peroxidase activity, but not the primary cause of the effect. *Suppression of TSH secretion* - **TSH (Thyroid Stimulating Hormone)** secretion is primarily regulated by negative feedback from thyroid hormones (T3 and T4) and TRH from the hypothalamus. - The Wolff-Chaikoff effect directly involves the thyroid gland's response to iodine and is not primarily mediated by TSH suppression. *Decreased conversion of T4 to T3* - The **conversion of T4 to T3** primarily occurs in peripheral tissues, mediated by deiodinase enzymes. - The Wolff-Chaikoff effect focuses on the inhibition of **iodine organification** and hormone release within the thyroid gland itself, not peripheral conversion.
Question 183: What is the normal range for the CSF/plasma glucose ratio?
- A. 1.2 - 1.6
- B. 0.6 - 0.8 (Correct Answer)
- C. 0.2 - 0.4
- D. 1.0 - 1.2
Explanation: ***Correct: 0.6 - 0.8*** - This ratio indicates that cerebrospinal fluid (CSF) glucose concentration is typically 60-80% of plasma glucose concentration - This range is crucial for identifying metabolic or infectious pathologies affecting the central nervous system - Normal CSF glucose is approximately 50-80 mg/dL when plasma glucose is 70-120 mg/dL *Incorrect: 0.2 - 0.4* - A ratio in this range indicates significantly low CSF glucose, suggesting conditions like bacterial meningitis or hypoglycorrhachia - This is well below the normal physiological proportion of glucose in the CSF relative to plasma - Seen in bacterial/tuberculous meningitis, fungal infections, or malignancy *Incorrect: 1.0 - 1.2* - A CSF/plasma glucose ratio close to or above 1.0 would imply that CSF glucose levels are equal to or higher than plasma levels, which is physiologically impossible under normal conditions - Glucose transport into the CSF is regulated by GLUT-1 transporters and typically results in lower concentrations than in plasma - The blood-brain barrier maintains this gradient *Incorrect: 1.2 - 1.6* - This range is even more exaggerated and physiologically impossible, as CSF glucose cannot exceed plasma glucose in a healthy individual - Such a high ratio would contradict the mechanisms of glucose transport across the blood-brain barrier - Would suggest laboratory error if observed
Question 184: Gas exchange in tissues takes place at?
- A. Artery
- B. Capillary (Correct Answer)
- C. Vein
- D. Venules
Explanation: ***Capillary*** - **Capillaries** are the smallest and most numerous blood vessels, with very thin walls (only one cell thick), which facilitates the efficient exchange of gases, nutrients, and waste products between blood and tissues. - Their extensive network ensures close proximity to nearly every cell in the body, maximizing the surface area and minimizing the diffusion distance for **gas exchange**. *Artery* - Arteries carry **oxygenated blood** away from the heart to the tissues but have thick, muscular walls designed for high pressure and transport, not for direct exchange with tissues. - They branch into smaller arterioles, which then lead to capillaries, making them a conduit rather than an exchange site. *Vein* - Veins carry **deoxygenated blood** back to the heart from the tissues and have relatively thin walls compared to arteries but are still too thick for efficient gas exchange. - They primarily serve as blood return vessels and reservoirs. *Venules* - Venules are small blood vessels that merge from capillaries and eventually combine to form veins; they primarily function in collecting blood from capillary beds. - While slightly more permeable than larger veins, their main role is still collection and transport, not the extensive gas exchange facilitated by capillaries.
Question 185: Transducin is a protein found in:
- A. Glomerulus
- B. Retina (Correct Answer)
- C. Skeletal muscle
- D. Adrenal medulla
Explanation: ***Retina*** - **Transducin** is a **G-protein** crucial for **phototransduction** in the retina. - It plays a key role in the cascade that converts light signals into electrical impulses within **rod** and **cone photoreceptor cells**. *Glomerulus* - The **glomerulus** is a capillary network in the **kidney** responsible for filtering blood. - Its primary proteins are involved in filtration barriers, such as **podocin** and **nephrin**, not transducin. *Skeletal muscle* - **Skeletal muscle** contains proteins like **actin**, **myosin**, and **troponins** for contraction. - Transducin is not involved in muscle contraction or skeletal muscle function. *Adrenal medulla* - The **adrenal medulla** produces **catecholamines** like epinephrine and norepinephrine. - Proteins in this gland are involved in hormone synthesis, storage, and release, not light perception.
Question 186: Substance that is completely reabsorbed from the kidney?
- A. Na+
- B. K+
- C. Urea
- D. Glucose (Correct Answer)
Explanation: ***Glucose*** - In a healthy individual, **virtually all filtered glucose** is reabsorbed in the proximal convoluted tubule via **sodium-glucose cotransporters (SGLTs)**. - This complete reabsorption ensures that this vital energy source is conserved and not excreted in the urine. *Na+* - While a large proportion of filtered **Na+** is reabsorbed to maintain fluid and electrolyte balance, not all of it is reabsorbed; some is excreted in urine. - The reabsorption of Na+ is **regulated** by hormones like **aldosterone** to fine-tune its excretion based on the body's needs. *K+* - **K+** undergoes both reabsorption and secretion in different parts of the nephron, and its excretion is tightly regulated. - Net reabsorption of K+ is not complete; its handling ensures appropriate plasma levels are maintained for muscle and nerve function. *Urea* - Approximately **50% of filtered urea undergoes reabsorption** in the renal tubules, while the other half is excreted. - Urea reabsorption is important for generating the **medullary osmotic gradient**, which is essential for concentrating urine, but it is never completely reabsorbed.
Question 187: During moderate exercise, the respiratory rate increases in response to which of the following?
- A. Increased PCO2 in arterial blood (Correct Answer)
- B. Proprioceptive feedback from muscle spindles
- C. Decreased PO2 in arterial blood
- D. Stimulation of J-receptors
Explanation: ***Increased PCO2 in arterial blood*** - This is the **marked correct answer**, though it requires clarification: during **moderate exercise**, **arterial PCO2** typically remains **stable** (~40 mmHg) because ventilation increases proportionally to CO2 production. - However, **central chemoreceptors** respond to even small oscillations in PCO2 and pH, and there is increased CO2 delivery to the respiratory center from **mixed venous blood**. - The **chemical stimulus** becomes more prominent during **intense exercise** when metabolic acidosis develops and arterial PCO2 may actually rise. - Note: The primary drivers during moderate exercise are **multifactorial**, including neural mechanisms (central command, proprioceptive feedback) and chemical factors working together. *Proprioceptive feedback from muscle spindles* - **Proprioceptors** from muscles and joints provide important **neurogenic drive** that contributes significantly to increased ventilation during moderate exercise. - This mechanism works alongside **central command** (feedforward signals from motor cortex) to initiate and sustain the ventilatory response. - While this is a major contributor, the question likely seeks the **chemical stimulus** as the "classical" answer, though modern physiology recognizes the integrated nature of exercise hyperpnea. *Decreased PO2 in arterial blood* - **Arterial PO2** typically remains **stable or increases slightly** during **moderate exercise** due to improved ventilation-perfusion matching and increased ventilation. - Significant hypoxemia triggering **peripheral chemoreceptors** occurs only during **strenuous exercise** (especially in untrained individuals), at high altitude, or in patients with cardiopulmonary disease. *Stimulation of J-receptors* - **J-receptors** (juxtacapillary receptors) in alveolar walls are stimulated by increased **pulmonary interstitial fluid**, such as in pulmonary edema or heart failure. - They cause **rapid, shallow breathing** and are not involved in the normal ventilatory response to moderate exercise.