Which of the following is an amino sugar formed from fructose-6-phosphate?
Which of the following is a true difference between gangliosides and cerebrosides?
The primary site of lipogenesis is:
Why is oxidized LDL considered more atherogenic?
Which of the following enzymes is not involved in the urea cycle?
Urea & Kreb's cycle are linked at?
Which will activate carbamoyl phosphate synthase I?
Ochronosis is due to accumulation of ?
Organ that can utilize glucose, fatty acids and ketone bodies is:
Which of the following is not the source of cytosolic NADPH ?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 91: Which of the following is an amino sugar formed from fructose-6-phosphate?
- A. N-acetylglucosamine-6-phosphate
- B. Glucosamine-6-phosphate (Correct Answer)
- C. Galactosamine-6-phosphate
- D. UDP-N-acetylglucosamine
Explanation: ***Glucosamine-6-phosphate*** - This amino sugar is directly synthesized from **fructose-6-phosphate** via a transamidation reaction, where an amino group replaces a hydroxyl group. - It is a key intermediate in the biosynthesis of other **amino sugars** and **glycosaminoglycans**. *N-acetylglucosamine-6-phosphate* - This is formed from **glucosamine-6-phosphate** by the addition of an **acetyl group**, making it a subsequent product, not the initial amino sugar from fructose-6-phosphate. - The N-acetylation step is crucial for its role in cellular signaling and structural components. *Galactosamine-6-phosphate* - While an amino sugar, **galactosamine-6-phosphate** is derived from UDP-N-acetylglucosamine, not directly from fructose-6-phosphate. - Its formation involves an **epimerization** step of an existing N-acetylglucosamine structure. *UDP-N-acetylglucosamine* - This is an **activated form** of N-acetylglucosamine, formed by the addition of UTP to N-acetylglucosamine-1-phosphate. - It serves as a precursor for the synthesis of complex **carbohydrates** and glycoproteins, far downstream from fructose-6-phosphate.
Question 92: Which of the following is a true difference between gangliosides and cerebrosides?
- A. Specific carbohydrate composition
- B. Charge difference (Correct Answer)
- C. Location in the nervous system
- D. Presence of glucose
Explanation: ***Charge difference*** - **Gangliosides** contain **sialic acid (N-acetylneuraminic acid)** residues, which are negatively charged, making gangliosides **anionic**. - **Cerebrosides** are **neutral glycosphingolipids** as they lack charged sugar residues. *Specific carbohydrate composition* - While both have carbohydrate components, referring to "specific carbohydrate composition" as the *true difference* is too broad. Both have characteristic sugar groups, but the **presence of sialic acid** in gangliosides is the key differentiator in charge. - Cerebrosides typically contain a single sugar (either glucose or galactose), whereas gangliosides have a more complex oligosaccharide chain including sialic acid. *Presence of glucose* - Both cerebrosides (specifically **glucocerebrosides**) and gangliosides can contain **glucose** in their carbohydrate moieties. - This is not a distinguishing feature; the *type* and *arrangement* of sugars, particularly the presence of sialic acid, are more specific. *Location in the nervous system* - Both gangliosides and cerebrosides are abundant in the **nervous system**, particularly in cell membranes. - Their presence in the nervous system is a similarity, not a differentiating factor.
Question 93: The primary site of lipogenesis is:
- A. Liver (Correct Answer)
- B. Skeletal muscles
- C. Myocardium
- D. Lungs
Explanation: ***Liver*** - The **liver** is the principal organ for **de novo lipogenesis**, converting excess carbohydrates into fatty acids and triglycerides. - This process is highly active in response to a high-carbohydrate diet, with the synthesized lipids packaged into **VLDL** for transport. *Skeletal muscles* - **Skeletal muscles** primarily utilize fatty acids for **energy production** rather than synthesizing large amounts of new lipids. - While they can store some triglycerides, their capacity for de novo lipogenesis is significantly lower compared to the liver. *Myocardium* - The **myocardium** (heart muscle) primarily relies on fatty acids for its continuous **energy demands** and has limited capacity for de novo lipogenesis. - Its metabolic focus is on efficient **ATP generation** to maintain cardiac function. *Lungs* - The **lungs** are not a primary site for general lipogenesis, though they are involved in the synthesis of specific lipids like **surfactant**. - Surfactant synthesis is a specialized process crucial for lung function, distinct from general energy storage lipogenesis.
Question 94: Why is oxidized LDL considered more atherogenic?
- A. Is not recognized by LDL receptors
- B. Is taken up by scavenger receptors (Correct Answer)
- C. Promotes inflammation in arterial walls
- D. Accumulates in macrophages
Explanation: ***Is taken up by scavenger receptors*** - **Oxidized LDL (oxLDL)** is taken up by **scavenger receptors (CD36, SR-A)** on macrophages, which have **no feedback regulation**. - Unlike native LDL receptors that downregulate when cells have sufficient cholesterol, **scavenger receptors continue unlimited uptake**, leading to foam cell formation. - This **unregulated uptake mechanism** is the key reason why oxLDL is **more atherogenic** than native LDL. - The result is lipid-laden macrophages forming **fatty streaks**, the initial lesions of **atherosclerosis**. *Is not recognized by LDL receptors* - While true that oxLDL has **reduced affinity** for native LDL receptors due to oxidative modification, this alone doesn't explain increased atherogenicity. - The critical factor is what happens instead—its uptake via an **alternative, unregulated pathway**. *Accumulates in macrophages* - This is a **consequence** of scavenger receptor uptake, not the primary mechanism. - Foam cell formation occurs **because** of unregulated scavenger receptor uptake, making this a downstream effect. *Promotes inflammation in arterial walls* - OxLDL does promote inflammation through multiple mechanisms (cytokine release, endothelial dysfunction). - However, this is a **secondary effect** that occurs after uptake and accumulation—not the primary reason for atherogenicity.
Question 95: Which of the following enzymes is not involved in the urea cycle?
- A. Arginase
- B. Argininosuccinate lyase
- C. CPS-II (Correct Answer)
- D. CPS-I
Explanation: ***CPS-II*** - Carbamoyl phosphate synthetase II is involved in **pyrimidine synthesis**, not the urea cycle. - It uses **glutamine** as a nitrogen donor and is located in the **cytosol**. *CPS-I* - Carbamoyl phosphate synthetase I is the **rate-limiting enzyme** of the urea cycle. - It catalyzes the formation of **carbamoyl phosphate** from **ammonia**, CO2, and ATP in the mitochondria. *Arginase* - Arginase is the **final enzyme** in the urea cycle, converting **arginine** to **ornithine** and **urea**. - This reaction occurs in the cytosol and releases urea for excretion. *Argininosuccinate lyase* - Argininosuccinate lyase catalyzes the cleavage of **argininosuccinate** into **fumarate** and **arginine**. - This is a key step in regenerating arginine for the final step of the urea cycle.
Question 96: Urea & Kreb's cycle are linked at?
- A. Arginine
- B. Ornithine
- C. Oxaloacetate
- D. Fumarate (Correct Answer)
Explanation: ***Fumarate*** - **Fumarate** is a key intermediate produced during the **urea cycle** when argininosuccinate is cleaved into arginine and fumarate. - This fumarate then enters the **Krebs cycle** (citric acid cycle) as an intermediate to be converted into malate and then oxaloacetate, thus linking the two cycles. *Arginine* - **Arginine** is an amino acid that participates in the urea cycle, serving as a precursor for the formation of urea. - While arginine is a part of the urea cycle, it does not directly enter the Krebs cycle or serve as its linking metabolite. *Ornithine* - **Ornithine** is another amino acid central to the urea cycle, being regenerated at the end of the cycle to combine with carbamoyl phosphate. - It is a carrier molecule for the nitrogen atoms, but it does not directly link to the Krebs cycle. *Oxaloacetate* - **Oxaloacetate** is a central intermediate in the Krebs cycle, and it can be a precursor for intermediates in the urea cycle (e.g., through aspartate). - However, it is not the direct molecule that links the two cycles in the direction of the urea cycle feeding into the Krebs cycle.
Question 97: Which will activate carbamoyl phosphate synthase I?
- A. N-acetyl glutamate (Correct Answer)
- B. ATP
- C. Acetyl-CoA
- D. Ornithine
Explanation: **N-acetyl glutamate** - **N-acetyl glutamate** is an **allosteric activator** of **carbamoyl phosphate synthase I (CPS I)**, which is the mitochondrial enzyme that catalyzes the first committed step of the **urea cycle**. - Its synthesis is stimulated by high levels of **arginine**, linking nitrogen load to urea production. *Acetyl-CoA* - Acetyl-CoA is a common **substrate** and **product** in various metabolic pathways, but it is not a direct activator of CPS I. - It is a precursor for the synthesis of **N-acetyl glutamate**, but does not activate CPS I directly. *Ornithine* - **Ornithine** is a key intermediate of the **urea cycle**, but it does not directly activate CPS I. - It combines with carbamoyl phosphate (the product of CPS I) in the second step of the urea cycle to form citrulline. *ATP* - **ATP** is a **substrate** used by CPS I to provide energy for the synthesis of carbamoyl phosphate. - While essential for the reaction, ATP itself does not act as an allosteric activator of the enzyme.
Question 98: Ochronosis is due to accumulation of ?
- A. Homogentisic acid (Correct Answer)
- B. Phenylpyruvate
- C. Xanthurenate
- D. Glyoxylate
Explanation: ***Homogentisic acid*** - Ochronosis is a condition caused by the excessive accumulation of **homogentisic acid** in connective tissues. - This accumulation occurs due to a deficiency of the enzyme **homogentisate 1,2-dioxygenase** (HGD), which is responsible for breaking down homogentisic acid in the tyrosine degradation pathway. *Phenylpyruvate* - **Phenylpyruvate** accumulates in **phenylketonuria (PKU)**, a different metabolic disorder where there's a deficiency in phenylalanine hydroxylase. - PKU leads to intellectual disability and other neurological problems, not the characteristic pigmentation and arthritis of ochronosis. *Xanthurenate* - **Xanthurenate** is an abnormal metabolite of tryptophan metabolism that can accumulate in **vitamin B6 deficiency**. - Its accumulation is associated with increased urinary excretion and is not directly implicated in the pathology of ochronosis. *Glyoxylate* - **Glyoxylate** is involved in various metabolic pathways, and its accumulation (or accumulation of its metabolic products like oxalate) is associated with **primary hyperoxaluria**. - Primary hyperoxaluria leads to kidney stones and kidney failure, a condition distinct from ochronosis.
Question 99: Organ that can utilize glucose, fatty acids and ketone bodies is:
- A. Liver
- B. Brain
- C. Skeletal muscle (Correct Answer)
- D. RBC
Explanation: ***Skeletal muscle*** - Skeletal muscle is highly adaptable and can utilize **glucose**, **fatty acids (FAs)**, and **ketone bodies** as fuel sources, especially during prolonged exercise or starvation. - Its metabolic flexibility allows it to switch between these substrates depending on their availability and the body's energy demands. *Liver* - The liver is central to metabolism but primarily **produces ketone bodies** from fatty acids rather than utilizing them as a major fuel source for its own energy needs. - While it uses glucose and FAs, its role in ketone body metabolism is largely synthetic. *Brain* - The brain preferentially uses **glucose** as its primary fuel. - During prolonged starvation, it can adapt to utilize **ketone bodies** as an alternative fuel source, but it does not significantly use fatty acids directly. *RBC* - Red blood cells (RBCs) lack mitochondria and therefore rely exclusively on **anaerobic glycolysis** for energy, metabolizing only **glucose**. - They cannot utilize fatty acids or ketone bodies.
Question 100: Which of the following is not the source of cytosolic NADPH ?
- A. Malic enzyme
- B. G6PD
- C. Isocitrate dehydrogenase
- D. ATP citrate lyase (Correct Answer)
Explanation: ***ATP citrate lyase*** - **ATP citrate lyase** is an enzyme involved in the synthesis of **acetyl-CoA** from citrate in the cytosol, which is then used for **fatty acid synthesis**. It does not generate NADPH. - While the **acetyl-CoA** produced is used in pathways that require NADPH, ATP citrate lyase itself does not directly produce NADPH. *Isocitrate dehydrogenase* - Cytosolic **isocitrate dehydrogenase** catalyzes the oxidative decarboxylation of **isocitrate** to alpha-ketoglutarate, producing **NADPH**. - This reaction is an important source of **cytosolic NADPH**, especially in non-photosynthetic tissues. *Malic enzyme* - **Malic enzyme** catalyzes the oxidative decarboxylation of **malate** to pyruvate, simultaneously reducing **NADP+ to NADPH**. - This enzyme is a significant source of **cytosolic NADPH** in various tissues, contributing to fatty acid synthesis and other reductive processes. *G6PD* - **Glucose-6-phosphate dehydrogenase (G6PD)** is the rate-limiting enzyme in the **pentose phosphate pathway** (PPP). - It catalyzes the first step of the PPP, converting **glucose-6-phosphate** to 6-phosphogluconolactone and producing **NADPH** as a crucial coenzyme.