Protein glycosylation occurs in:
Which isoform of LDH is raised in Anemia ?
Which molecule serves as the ultimate source of acetyl groups for fatty acid synthesis?
What is the role of Apoprotein C-II in lipid metabolism?
In a person fasting overnight with carnitine deficiency, which of the following chemicals increase in quantity in blood?
Indole ring is present in?
Transamination of Alanine results in formation of ?
Which of the following statements about protein denaturation is correct?
Major source of energy for brain in fasting/starvation?
What is the primary product of fatty acid oxidation (β-oxidation)?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 141: Protein glycosylation occurs in:
- A. Peroxisomes
- B. Endoplasmic reticulum (ER) (Correct Answer)
- C. Mitochondria
- D. Golgi bodies
Explanation: ***ER*** - **N-linked glycosylation**, the most common type of protein glycosylation, initiates in the **endoplasmic reticulum (ER)**, where an oligosaccharide precursor is transferred to asparagine residues of newly synthesized proteins. - The ER environment facilitates protein folding and quality control, ensuring correctly folded glycoproteins are transported further. *Golgi bodies* - While **further modification and processing** of glycosylated proteins occur in the Golgi apparatus, the initial step of N-linked glycosylation begins in the ER. - The Golgi is responsible for trimming and adding different sugar residues to complete the **glycan chains** and for sorting the glycoproteins to their final destinations. *Mitochondria* - Mitochondria are primarily involved in **cellular respiration** and **ATP production**. - They do not play a significant role in protein glycosylation; most mitochondrial proteins are imported from the cytoplasm in an unglycosylated state. *Peroxisomes* - Peroxisomes are involved in various **metabolic processes**, including fatty acid oxidation and detoxification. - They are not known to be sites of protein glycosylation.
Question 142: Which isoform of LDH is raised in Anemia ?
- A. LDH 5
- B. LDH 4
- C. LDH 1
- D. LDH 2 (Correct Answer)
Explanation: ***Correct: LDH 2*** - **LDH 2 (H3M1)** is highly abundant in **red blood cells (RBCs)**, second only to LDH 1. - In **hemolytic anemia**, there is increased destruction of red blood cells, leading to the release of intracellular LDH isoforms into the bloodstream. - Both **LDH 1 and LDH 2 are significantly elevated** in hemolytic anemia, as RBCs contain predominantly these two isoforms. - The elevation of LDH 2 is particularly notable and diagnostically useful in anemia, especially hemolytic conditions. *Incorrect: LDH 1* - **LDH 1 (H4)** is the most abundant isoform in **heart muscle** and is also present in **red blood cells**. - While LDH 1 is indeed elevated in hemolytic anemia, this option is not the best answer in this context. - LDH 1 elevation is classically associated with **myocardial infarction**. *Incorrect: LDH 4* - **LDH 4 (HM3)** is present in various tissues, including **liver, skeletal muscle, and kidneys**, but in lower concentrations. - Not the primary isoform associated with anemia. *Incorrect: LDH 5* - **LDH 5 (M4)** is predominantly found in the **liver and skeletal muscles**. - Elevation of LDH 5 typically indicates **liver damage, muscle injury, or malignancies**, not primarily anemia.
Question 143: Which molecule serves as the ultimate source of acetyl groups for fatty acid synthesis?
- A. Malonyl CoA
- B. Palmitate
- C. Acetyl CoA (Correct Answer)
- D. Citrate
Explanation: ***Acetyl CoA*** - **Acetyl CoA** is the ultimate source of all acetyl groups used in fatty acid synthesis - It serves as the substrate for **acetyl CoA carboxylase**, which converts it to **malonyl CoA** - After transport from mitochondria via **citrate**, acetyl CoA is the precursor for all two-carbon units incorporated into fatty acids - One molecule of acetyl CoA also serves as the primer for fatty acid synthesis *Malonyl CoA* - **Malonyl CoA** is the direct two-carbon donor to the growing fatty acid chain - However, it is derived from **acetyl CoA** through carboxylation by **acetyl CoA carboxylase** - It is an intermediate, not the ultimate source of acetyl groups *Palmitate* - **Palmitate** is a 16-carbon saturated fatty acid that is the end product of de novo fatty acid synthesis - It is the product of fatty acid synthesis, not a donor of acetyl groups *Citrate* - **Citrate** transports acetyl groups from the **mitochondria** to the **cytosol** where fatty acid synthesis occurs - In the cytosol, **ATP citrate lyase** cleaves citrate back into **acetyl CoA** and oxaloacetate - Citrate is a transport vehicle, not the ultimate source of acetyl groups
Question 144: What is the role of Apoprotein C-II in lipid metabolism?
- A. None of the options
- B. Inhibits lipoprotein lipase
- C. Facilitates triglyceride transport
- D. Activates lipoprotein lipase (Correct Answer)
Explanation: ***Activates lipoprotein lipase*** - **Apoprotein C-II (ApoC-II)** is a crucial **activator** of **lipoprotein lipase (LPL)**. - LPL is an enzyme responsible for **hydrolyzing triglycerides** from chylomicrons and VLDL, allowing fatty acids to be taken up by tissues. - **Deficiency of ApoC-II** leads to severe hypertriglyceridemia due to inability to activate LPL. *Inhibits lipoprotein lipase* - This is the function of **ApoC-III**, not ApoC-II. - ApoC-III **inhibits LPL activity**, which is the opposite role of ApoC-II. *Facilitates triglyceride transport* - While apoproteins are essential for **assembly and transport of lipoproteins** that carry triglycerides, this is not the specific primary role of ApoC-II. - ApoC-II's primary function is **regulating LPL enzyme activity**, not direct transport facilitation. *None of the options* - This is incorrect because ApoC-II clearly **activates lipoprotein lipase**, which is one of the given options.
Question 145: In a person fasting overnight with carnitine deficiency, which of the following chemicals increase in quantity in blood?
- A. Ketone body levels
- B. Fatty acid levels (Correct Answer)
- C. Glucose levels
- D. Amino acid levels
Explanation: ***Fatty acid levels*** - **Carnitine deficiency** impairs the transport of **long-chain fatty acids** into the mitochondria for beta-oxidation. - This leads to an accumulation of **fatty acids** in the blood as they cannot be efficiently metabolized for energy during fasting. - Therefore, **fatty acid levels increase** in the blood. *Ketone body levels* - **Ketone bodies** are produced from the **beta-oxidation of fatty acids** in the liver. - With **carnitine deficiency**, fatty acid oxidation is impaired, thus **reducing** the production of ketone bodies, not increasing them. *Glucose levels* - During **fasting**, the body relies on **gluconeogenesis** and **glycogenolysis** to maintain glucose levels. - With carnitine deficiency primarily affecting fat metabolism and preventing fatty acid utilization, the body cannot spare glucose effectively. - This leads to **hypoglycemia** (decreased glucose), not increased glucose levels. *Amino acid levels* - **Amino acid metabolism** is largely independent of **carnitine**. - While amino acids can be used for gluconeogenesis during fasting, carnitine deficiency does not directly cause an increase in circulating amino acid levels.
Question 146: Indole ring is present in?
- A. Tryptophan (Correct Answer)
- B. Tyrosine
- C. Phenylalanine
- D. Threonine
Explanation: ***Tryptophan*** - Tryptophan is an **aromatic amino acid** characterized by the presence of an **indole ring** in its side chain. - The indole ring consists of a **benzene ring fused to a pyrrole ring**, which is unique to tryptophan among the standard amino acids. *Tyrosine* - Tyrosine is an **aromatic amino acid** containing a **phenol group** (a benzene ring with a hydroxyl group), not an indole ring. - It is derived from phenylalanine and is a precursor for important molecules like **thyroid hormones** and **catecholamines**. *Phenylalanine* - Phenylalanine is an **aromatic amino acid** with a **benzyl group** (a benzene ring attached to a methylene group) in its side chain. - It lacks the distinct heterocyclic indole structure found in tryptophan. *Threonine* - Threonine is an **aliphatic amino acid** with a **hydroxyl group** on its side chain, classifying it as a **polar, uncharged amino acid**. - It does not contain any ring structures, especially not an indole ring.
Question 147: Transamination of Alanine results in formation of ?
- A. Oxaloacetate
- B. Pyruvate (Correct Answer)
- C. Aspartate
- D. Arginine
Explanation: **Pyruvate** ✓ - **Transamination** involves the transfer of an amino group from an amino acid to an α-ketoglutarate (catalyzed by aminotransferases). - When **alanine** undergoes transamination via **ALT (alanine aminotransferase)**, its amino group is transferred to α-ketoglutarate, forming glutamate, while alanine is converted to its corresponding α-keto acid, which is **pyruvate**. - Reaction: Alanine + α-Ketoglutarate ⇄ Pyruvate + Glutamate *Oxaloacetate* - **Oxaloacetate** is the α-keto acid formed from the transamination of **aspartate** (via AST/GOT). - It is a key intermediate in the **citric acid cycle** and gluconeogenesis, not a product of alanine transamination. *Aspartate* - **Aspartate** is an amino acid, not an α-keto acid. - It can be formed from oxaloacetate via transamination (reverse reaction), and is involved in the **urea cycle** and nucleotide synthesis. *Arginine* - **Arginine** is a semi-essential amino acid, not an α-keto acid or a product of alanine transamination. - It plays roles in **protein synthesis**, the urea cycle, and nitric oxide production.
Question 148: Which of the following statements about protein denaturation is correct?
- A. Biological properties are retained after denaturation.
- B. Denaturation is always irreversible.
- C. The primary structure of the protein is unaffected. (Correct Answer)
- D. Denaturation never results in proteins becoming insoluble.
Explanation: ***The primary structure of the protein is unaffected.*** - Denaturation refers to the disruption of a protein's **secondary, tertiary, and quaternary structures**, while the **covalent peptide bonds** that form the primary structure remain intact. - The sequence of amino acids, which defines the primary structure, is not typically altered by denaturing agents such as heat, pH changes, or chemicals. *Biological properties are retained after denaturation.* - Denaturation typically leads to the **loss of a protein's specific three-dimensional shape**, which is essential for its biological function. - Therefore, the biological properties and **activity of the protein are usually lost** or significantly impaired upon denaturation. *Denaturation is always irreversible.* - While many cases of denaturation are irreversible (e.g., cooking an egg), some proteins can **renature** if the denaturing conditions are removed, restoring their original structure and function. - This reversibility depends on the **severity and duration of the denaturing agent**, as well as the protein's inherent stability. *Denaturation never results in proteins becoming insoluble.* - Denaturation often exposes **hydrophobic regions** of a protein that were previously buried within its folded structure, leading to aggregation and **precipitation**, thereby making the protein insoluble. - This insolubility is a common consequence of denaturation, particularly with significant structural disruption.
Question 149: Major source of energy for brain in fasting/starvation?
- A. Glucose
- B. Glycogen
- C. Fatty acids
- D. Ketone bodies (Correct Answer)
Explanation: ***Ketone bodies*** - During **prolonged fasting or starvation**, the body depletes its **glycogen stores** and begins to break down fatty acids. The liver converts these fatty acids into **ketone bodies**, such as **acetoacetate and beta-hydroxybutyrate**. - These **ketone bodies** can cross the **blood-brain barrier** and be used by the brain as an alternative energy source when glucose becomes scarce, preventing protein breakdown for gluconeogenesis. *Glucose* - While **glucose** is the primary and preferred energy source for the brain under normal physiological conditions, its availability significantly decreases during **prolonged fasting or starvation**. - The brain requires a continuous supply of glucose, but in states of severe caloric restriction, the body must conserve glucose for other critical functions and adapt by using alternative fuels. *Glycogen* - **Glycogen** is a stored form of glucose found predominantly in the **liver and muscles**. - The brain itself has minimal **glycogen stores**, which are rapidly depleted during fasting, and thus cannot be a major long-term energy source. *Fatty acids* - **Fatty acids** are a major energy source for many tissues in the body, especially during fasting, but they **cannot directly cross the blood-brain barrier** in significant amounts to fuel the brain. - Instead, **fatty acids** are metabolized into **ketone bodies** in the liver, which then serve as the brain's alternative fuel.
Question 150: What is the primary product of fatty acid oxidation (β-oxidation)?
- A. Acetyl CoA (Correct Answer)
- B. Malonyl CoA
- C. Ketone bodies
- D. Cholesterol
Explanation: ***Acetyl CoA*** - Beta-oxidation of fatty acids involves a series of reactions that cleave two-carbon units from the fatty acyl chain, forming **acetyl CoA**. - **Acetyl CoA** is the direct product of each cycle of β-oxidation and then enters the **citric acid cycle** to generate ATP or serves as a precursor for other anabolic pathways. *Malonyl CoA* - **Malonyl CoA** is a key intermediate in **fatty acid synthesis**, not degradation. - It's formed from acetyl CoA by acetyl-CoA carboxylase and acts as a substrate for **fatty acid synthase**, and also as a physiological inhibitor of carnitine palmitoyltransferase I (CPT-I), thereby regulating β-oxidation. *Ketone bodies* - **Ketone bodies** (**acetoacetate** and **β-hydroxybutyrate**) are produced from acetyl CoA in the liver during conditions of low glucose availability or prolonged fasting. - They serve as an alternative fuel source for tissues like the brain and muscles, but are secondary products derived from the condensation of acetyl CoA molecules, not the primary direct product of fatty acid breakdown itself. *Cholesterol* - **Cholesterol** is a steroid lipid synthesized from **acetyl CoA** through a complex multi-step pathway (via HMG-CoA reductase pathway). - It is an important structural component of cell membranes and a precursor for steroid hormones and bile acids, but not a direct product of fatty acid catabolism.