NEET-PG 2012 Practice Questions

Q: Which of the following statements about chylomicrons is true?

Chylomicrons primarily contain triglycerides (TGs).. ***Chylomicrons primarily contain triglycerides (TGs)*** - **Chylomicrons** are the largest and least dense lipoproteins, primarily responsible for transporting **dietary triglycerides** absorbed from the intestine to peripheral tissues. - They are synthesized in the **enterocytes** of the small intestine and released into the lymphatic system. - Approximately **85-90%** of a chylomicron's mass is composed of **triglycerides**, making them the primary carriers of exogenous fats. *Chylomicrons primarily contain cholesterol* - While chylomicrons do contain some **cholesterol**, it is a minor component (~3-5%) compared to their predominant content, which is **triglycerides**. - Lipoproteins like **LDL** and **HDL** are primarily responsible for cholesterol transport. *Chylomicrons are unrelated to triglyceride transport* - This statement is incorrect; chylomicrons are fundamentally involved in the **transport of dietary triglycerides** from the intestines to various tissues in the body. - After lipoprotein lipase acts on chylomicrons in peripheral tissues, triglycerides are hydrolyzed and fatty acids are taken up by tissues. *Chylomicrons do not primarily contain triglycerides* - This statement directly contradicts the main function and composition of chylomicrons, which are **rich in triglycerides**. - Without triglycerides as their primary content, chylomicrons would not be able to fulfill their physiological role in lipid transport.

Q: Which enzyme is primarily responsible for the fat metabolism in adipose tissue?

Hormone-sensitive lipase. ***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.

Q: Enzyme deficient in Type I Hyperlipidemia?

Lipoprotein lipase. ***Lipoprotein lipase*** - **Type I hyperlipidemia**, also known as **familial hyperchylomicronemia**, is characterized by a deficiency in **lipoprotein lipase (LPL)**. - LPL is crucial for hydrolyzing triglycerides in **chylomicrons** and **VLDLs** into fatty acids and glycerol, allowing their uptake by tissues. *HMG CoA reductase* - This enzyme is involved in the **rate-limiting step of cholesterol synthesis** in the liver. - While it plays a role in lipid metabolism, its deficiency is not characteristic of **Type I hyperlipidemia**. *Peroxidase* - **Peroxidase** is an enzyme involved in various oxidative reactions, including the breakdown of **hydrogen peroxide**. - It is not directly involved in the metabolism of **chylomicrons** or **triglycerides**, and its deficiency is unrelated to hyperlipidemia. *Cholesterol acyl transferase* - This enzyme, often referring to **lecithin-cholesterol acyltransferase (LCAT)** or **acyl-CoA:cholesterol acyltransferase (ACAT)**, is involved in **cholesterol esterification**. - While important for cholesterol transport and storage, its deficiency is not the primary cause of **Type I hyperlipidemia**, which is marked by severe **chylomicronemia**.

Q: Taurine is biosynthesized from which amino acid?

Cysteine. ***Cysteine*** - **Taurine** is primarily synthesized from the amino acid **cysteine** through a pathway involving **cysteine sulfinic acid** and **hypotaurine**. - This pathway utilizes enzymes like **cysteine dioxygenase** and **cysteine sulfinic acid decarboxylase**. - The biosynthetic pathway: Cysteine → Cysteine sulfinic acid → Hypotaurine → Taurine. *Arginine* - **Arginine** is a precursor for **nitric oxide**, **urea**, and **creatine**, not taurine. - It is involved in various metabolic pathways, including the **urea cycle** and protein synthesis. *Valine* - **Valine** is a **branched-chain amino acid (BCAA)** involved in protein synthesis and energy production. - It is not a direct precursor for taurine biosynthesis. *Leucine* - **Leucine** is also a **branched-chain amino acid (BCAA)** crucial for protein synthesis and muscle metabolism. - It does not participate in the synthesis of taurine.

Q: Selenocysteine is associated with ?

Deiodinase. ***Deiodinase*** - Selenocysteine is a critical component of **iodothyronine deiodinases**, a family of enzymes that regulate **thyroid hormone metabolism**. - These enzymes catalyze the removal of iodine from thyroid hormones, converting **thyroxine (T4)** into the more active **triiodothyronine (T3)** or inactive forms. *Carbonic anhydrase* - This enzyme contains **zinc** as its essential metal cofactor and is involved in the interconversion of **carbon dioxide** and **bicarbonate**. - Its primary role is in pH regulation and CO2 transport, without any direct association with selenocysteine. *Catalase* - Catalase is an enzyme primarily found in **peroxisomes** and contains **iron-porphyrin** groups as its prosthetic group. - Its function is to convert **hydrogen peroxide** into water and oxygen, protecting cells from oxidative damage. *Transferase* - Transferases are a broad class of enzymes that catalyze the transfer of **functional groups** (e.g., methyl, glucose) from one molecule to another. - While essential for many metabolic processes, there is no inherent association of the general class of transferases with selenocysteine.

Q: Carnitine is synthesised from -

Lysine. ***Lysine*** - **Carnitine** is synthesized in the liver and kidneys from the amino acids **lysine** and methionine. - **Lysine provides the essential carbon backbone** for carnitine synthesis (trimethyllysine is the actual precursor formed from protein-bound lysine residues). - Methionine contributes methyl groups via S-adenosylmethionine (SAM), but lysine is the primary structural precursor. *Arginine* - **Arginine** is a precursor for **nitric oxide**, urea, and creatine, but not a direct precursor for carnitine synthesis. - While arginine is an amino acid, its metabolic pathways are distinct from those involved in carnitine formation. *Histidine* - **Histidine** is a precursor for **histamine** and contributes to protein synthesis, but is not involved in carnitine biosynthesis. - Its metabolic fate differs significantly from the pathway leading to carnitine. *Choline* - **Choline** is a precursor for **acetylcholine** and phospholipids, but not directly for carnitine. - Although both choline and carnitine contain methyl groups, they have different biosynthetic origins.

Q: Which cofactor is primarily associated with the activity of glutamate dehydrogenase?

NAD+. ***NAD+*** - Glutamate dehydrogenase catalyzes the oxidative deamination of **glutamate** to **α-ketoglutarate** and ammonia, and this reaction primarily uses **NAD+** as an electron acceptor. - In some organisms and contexts, it can also use **NADP+**, but **NAD+** is the more common and significant cofactor for its catabolic role. *FAD* - **FAD (flavin adenine dinucleotide)** is typically associated with **flavoproteins** and enzymes involved in oxidation-reduction reactions, such as those in the **electron transport chain** and the **Krebs cycle**. - Enzymes like **succinate dehydrogenase** use FAD, not glutamate dehydrogenase. *FMN* - **FMN (flavin mononucleotide)** is another flavin coenzyme, similar to FAD, and is found in various **flavoproteins** and enzymes of the **electron transport chain**, such as **NADH dehydrogenase (Complex I)**. - It does not serve as a primary cofactor for **glutamate dehydrogenase** activity. *FADH2* - **FADH2** is the reduced form of **FAD**, carrying high-energy electrons to the **electron transport chain** for ATP synthesis. - It's a product or reactant of various metabolic pathways, but not a direct cofactor for **glutamate dehydrogenase**.

Q: What is the primary biochemical defect in alkaptonuria?

Deficiency of homogentisate 1,2-dioxygenase. ***Deficiency of homogentisate 1,2-dioxygenase*** - **Alkaptonuria** is an autosomal recessive disorder caused by the deficiency of **homogentisate 1,2-dioxygenase**, an enzyme in the **tyrosine degradation pathway**. - This deficiency leads to the accumulation of **homogentisic acid** in the body, which is excreted in urine and deposited in connective tissues. *Urine turns black immediately upon voiding* - While urine in alkaptonuria does **turn black**, it typically darkens upon **standing** and exposure to air, not immediately upon voiding. - The darkening is due to the oxidation of accumulated **homogentisic acid**. *FeCl3 test is negative* - The **ferric chloride (FeCl3) test** typically yields a **positive result** (transient green color) in the presence of homogentisic acid in the urine. - Therefore, a negative result would argue against a diagnosis of alkaptonuria. *Benedict's test is diagnostic for alkaptonuria* - **Benedict's test** is used to detect reducing sugars like glucose in urine and would not be used to diagnose alkaptonuria. - A positive Benedict's test in alkaptonuria is due to the reducing properties of homogentisic acid, but it is not specific or diagnostic.

Q: What is the body's first physiological response to hypoglycemia?

Decreased insulin. ***Decreased insulin*** - **Decreased insulin secretion** is the body's **first and earliest** physiological response to falling blood glucose levels, occurring at approximately **80-85 mg/dL**. - This represents the **primary defense mechanism** against hypoglycemia - by reducing insulin release from pancreatic beta cells, the body removes the most potent glucose-lowering stimulus. - This allows blood glucose to stabilize before it drops further, and occurs **before** any active counterregulatory hormones are released. - This is a critical **first-line defense** that prevents the need for more aggressive counterregulatory responses. *Increased glucagon* - **Glucagon** is the **second line of defense** against hypoglycemia, with secretion increasing at glucose levels around **65-70 mg/dL**. - While glucagon is the most important **active counterregulatory hormone** (stimulating glycogenolysis and gluconeogenesis), it is not the *first* response. - The temporal sequence is: insulin suppression occurs first, followed by glucagon release if glucose continues to fall. *Increased cortisol* - **Cortisol** is a late counterregulatory hormone, responding to more severe or prolonged hypoglycemia (glucose <65 mg/dL). - It promotes gluconeogenesis and reduces peripheral glucose utilization over hours, not minutes. - Along with growth hormone, cortisol provides sustained glucose elevation but is not an early response. *Increased norepinephrine* - **Norepinephrine** (and epinephrine) are part of the sympathetic/adrenomedullary response to hypoglycemia at approximately **65-70 mg/dL**. - These catecholamines provide important counterregulation but are activated after insulin suppression has already occurred. - They contribute to both glucose mobilization and the symptomatic (adrenergic) response to hypoglycemia.

Question 1

Which of the following statements about chylomicrons is true?

Accepted Answer

Chylomicrons primarily contain triglycerides (TGs).

Answer

Chylomicrons are unrelated to triglyceride transport.

Answer

Chylomicrons primarily contain cholesterol.

Answer

Chylomicrons do not primarily contain triglycerides.

Question 2

Which enzyme is primarily responsible for the fat metabolism in adipose tissue?

Accepted Answer

Hormone-sensitive lipase

Answer

Lipoprotein lipase

Answer

Acid lipase

Answer

Acid maltase

Question 3

Enzyme deficient in Type I Hyperlipidemia?

Accepted Answer

Lipoprotein lipase

Answer

HMG CoA reductase

Answer

Peroxidase

Answer

Cholesterol acyl transferase

Question 4

Taurine is biosynthesized from which amino acid?

Accepted Answer

Cysteine

Answer

Valine

Answer

Arginine

Answer

Leucine

Question 5

Selenocysteine is associated with ?

Accepted Answer

Deiodinase

Answer

Carbonic anhydrase

Answer

Catalase

Answer

Transferase

Question 6

Carnitine is synthesised from -

Accepted Answer

Lysine

Answer

Histidine

Answer

Choline

Answer

Arginine

Question 7

Which cofactor is primarily associated with the activity of glutamate dehydrogenase?

Accepted Answer

NAD+

Answer

FAD

Answer

FMN

Answer

FADH2

Question 8

What is the primary biochemical defect in alkaptonuria?

Accepted Answer

Deficiency of homogentisate 1,2-dioxygenase

Answer

FeCl3 test is negative

Answer

Urine turns black immediately upon voiding

Answer

Benedict's test is diagnostic for alkaptonuria

Question 9

Which one of the following statements concerning gluconeogenesis is correct?

Accepted Answer

It is important in maintaining blood glucose during the normal overnight fast.

Answer

It occurs primarily in the liver.

Answer

It is stimulated by elevated levels of acetyl CoA.

Answer

It is primarily inhibited by insulin.

Question 10

What is the body's first physiological response to hypoglycemia?

Accepted Answer

Decreased insulin

Answer

Increased glucagon

Answer

Increased cortisol

Answer

Increased norepinephrine

NEET-PG 2012

Biochemistry

Physiology