Major source of energy for brain in fasting/starvation?
What is the primary product of fatty acid oxidation (β-oxidation)?
Which of the following is a Fat Soluble vitamin?
Pyridoxine deficiency leads to altered metabolism of?
The Shine-Dalgarno sequence is primarily associated with which biological process?
What is the primary function of a primer in DNA replication?
In which stage of cell division is chromosomal study best carried out?
Who invented the technique for identifying individuals by their DNA?
Acute intermittent porphyria is due to deficiency of?
What is the primary metal ion found in myoglobin?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 101: 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 102: 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.
Question 103: Which of the following is a Fat Soluble vitamin?
- A. Thiamine
- B. Vitamin A (Correct Answer)
- C. Niacin
- D. Riboflavin
Explanation: ***Vitamin A*** - **Vitamin A** is one of the four essential **fat-soluble vitamins** (A, D, E, K), meaning it dissolves in fat and is stored in the body's fatty tissues and liver. - Its **absorption** relies on dietary fats and bile salts, distinguishing it from water-soluble vitamins. *Thiamine* - **Thiamine** (Vitamin B1) is a **water-soluble vitamin** that plays a crucial role in metabolism, converting carbohydrates into energy. - It is **not stored** in large amounts in the body and needs to be replenished regularly through diet. *Niacin* - **Niacin** (Vitamin B3) is a **water-soluble vitamin** vital for cellular metabolism, involving in DNA repair and steroid hormone synthesis. - It is readily excreted in urine when consumed in excess and does not accumulate in fatty tissues. *Riboflavin* - **Riboflavin** (Vitamin B2) is a **water-soluble vitamin** essential for energy production, cellular function, and the metabolism of fats, drugs, and steroids. - Like other B vitamins, it has limited storage in the body and is not dissolved in fat.
Question 104: Pyridoxine deficiency leads to altered metabolism of?
- A. Phenylalanine
- B. Methionine
- C. Tyrosine
- D. Tryptophan (Correct Answer)
Explanation: ***Tryptophan*** - **Pyridoxine (vitamin B6)** is a critical coenzyme in the metabolism of **tryptophan**, particularly in its conversion to **niacin** and serotonin. - A deficiency leads to an accumulation of abnormal tryptophan metabolites, such as **xanthurenic acid**, which can be excreted in the urine. *Phenylalanine* - The metabolism of phenylalanine involves its conversion to tyrosine, a process catalyzed by **phenylalanine hydroxylase**, which does not directly require pyridoxine. - Deficiencies in phenylalanine metabolism often point to issues like **phenylketonuria**. *Methionine* - Methionine metabolism involves a cycle that generates **S-adenosylmethionine (SAM)** and then homocysteine. - While vitamin B6 is involved in the transsulfuration pathway (converting homocysteine to cysteine), its primary direct impact on methionine metabolism itself is less pronounced than on tryptophan. *Tyrosine* - Tyrosine is synthesized from phenylalanine and is a precursor for **catecholamines** and thyroid hormones. - Its metabolism does not directly rely on pyridoxine as a coenzyme in the main initial steps.
Question 105: The Shine-Dalgarno sequence is primarily associated with which biological process?
- A. Transcription
- B. Translation (Correct Answer)
- C. DNA replication
- D. RNA splicing
Explanation: ***Translation*** - The **Shine-Dalgarno sequence** is a **ribosome-binding site** in prokaryotic messenger RNA (mRNA) that helps recruit the ribosome to the mRNA to initiate protein synthesis. - Its interaction with the **16S rRNA** of the small ribosomal subunit positions the start codon (AUG) correctly for **translation initiation**. - This sequence is located approximately **8 base pairs upstream** of the start codon in bacterial mRNA. *Transcription* - **Transcription** is the process of synthesizing RNA from a DNA template. - It involves elements like **promoters** and **enhancers**, not the Shine-Dalgarno sequence. *DNA replication* - **DNA replication** is the process by which DNA makes a copy of itself. - This process involves origins of replication, helicases, and DNA polymerases, with no role for the Shine-Dalgarno sequence. *RNA splicing* - **RNA splicing** is a eukaryotic process that removes introns from pre-mRNA. - The Shine-Dalgarno sequence is found in **prokaryotes**, which lack splicing machinery and introns.
Question 106: What is the primary function of a primer in DNA replication?
- A. Transcription
- B. Translation
- C. Initiation of DNA replication (Correct Answer)
- D. Termination of DNA replication
Explanation: ***Initiation of DNA replication*** - DNA polymerase cannot synthesize new DNA strands de novo; it requires a pre-existing 3'-hydroxyl group to begin adding nucleotides. - The **primer**, a short RNA sequence, provides this necessary **3'-hydroxyl group**, allowing DNA polymerase to start synthesizing the new DNA strand. *Transcription* - This process involves synthesizing **RNA from a DNA template**, primarily carried out by **RNA polymerase**. - While primers are involved in DNA synthesis, they do not directly initiate the process of transcription. *Translation* - **Translation** is the process of synthesizing **proteins from mRNA templates** using ribosomes, tRNA, and amino acids. - This process is distinct from DNA synthesis and does not involve primers; its initiation involves start codons and ribosomal subunits. *Termination of DNA replication* - **Termination of DNA replication** occurs when replication forks meet or at specific termination sequences, often with the involvement of specialized proteins. - Primers are involved in the *start* of replication, not its conclusion.
Question 107: In which stage of cell division is chromosomal study best carried out?
- A. Metaphase (Correct Answer)
- B. Telophase
- C. Anaphase
- D. Prophase
Explanation: ***Metaphase*** - During **metaphase**, chromosomes are maximally condensed and align at the cell's equatorial plate, making them easily visible and distinguishable under a microscope. - This arrangement allows for clear visualization of **chromosome number**, **size**, and **morphology**, which is crucial for genetic analysis. *Prophase* - In **prophase**, chromosomes begin to condense, but they are still diffuse and not fully compact, making detailed study difficult. - The nuclear envelope is also still present for most of prophase, obstructing a clear view of the chromosomes. *Telophase* - During **telophase**, chromosomes decondense and arrive at opposite poles, becoming less distinct and harder to analyze individually. - New nuclear envelopes form around the separated chromosomes, further obscuring their view for detailed study. *Anaphase* - In **anaphase**, sister chromatids separate and move towards opposite poles, but they are in motion and not aligned, making them difficult to capture and analyze individually. - The separated chromatids are also stretched and elongated, which makes their morphological assessment challenging.
Question 108: Who invented the technique for identifying individuals by their DNA?
- A. Shapiro
- B. Lewis
- C. Jeffreys (Correct Answer)
- D. Pasteur
Explanation: ***Jeffreys*** - **Alec Jeffreys** developed the technique of **DNA fingerprinting** in 1984, which revolutionized forensic science and paternity testing. - His method involved analyzing **variable number tandem repeats (VNTRs)** in DNA to create a unique profile for each individual. *Shapiro* - **Robert Shapiro** is a legal figure, famously associated with the O. J. Simpson murder trial, not directly with the invention of DNA identification techniques. - While he was involved in cases where DNA evidence was used, he did not contribute to its scientific development. *Lewis* - **Edward B. Lewis** was a Nobel Prize-winning geneticist known for his work on **developmental genetics** in *Drosophila melanogaster*, not for DNA identification techniques. - His research focused on gene clusters and their role in embryonic development. *Pasteur* - **Louis Pasteur** was a pioneering microbiologist and chemist, famous for his discoveries related to **vaccination**, microbial fermentation, and pasteurization. - His work predates the discovery and application of DNA for individual identification by over a century.
Question 109: Acute intermittent porphyria is due to deficiency of?
- A. Porphobilinogen deaminase (Correct Answer)
- B. Uroporphyrinogen III synthase
- C. Ferrochelatase
- D. ALA synthase
Explanation: ***Porphobilinogen deaminase*** - **Acute intermittent porphyria (AIP)** results from a deficiency in **porphobilinogen deaminase** (also known as hydroxymethylbilane synthase). - This enzyme deficiency leads to the accumulation of **aminolevulinic acid (ALA)** and **porphobilinogen (PBG)**, which are neurotoxic and cause the characteristic symptoms of AIP. *Uroporphyrinogen III synthase* - A deficiency in **uroporphyrinogen III synthase** causes **congenital erythropoietic porphyria (Günther disease)**, which is characterized by severe photosensitivity and hemolytic anemia. - This enzyme defect leads to the accumulation of uroporphyrinogen I and coproporphyrinogen I, not the ALA and PBG associated with AIP. *Ferrochelatase* - Deficiency in **ferrochelatase** causes **erythropoietic protoporphyria (EPP)**, which presents with photosensitivity and chronic liver disease due to the accumulation of **protoporphyrin**. - This condition does not cause the acute neurological attacks seen in AIP. *ALA synthase* - **ALA synthase** is the **rate-limiting enzyme** in heme synthesis; while its activity is crucial, a congenital *deficiency* is not the cause of AIP. - Instead, the *upregulation* of ALA synthase activity in AIP (due to the PBG deaminase block) contributes to the accumulation of ALA and PBG.
Question 110: What is the primary metal ion found in myoglobin?
- A. Iron (Correct Answer)
- B. Copper
- C. Selenium
- D. Zinc
Explanation: ***Iron*** - **Iron** is the central metal ion in the **heme group** of myoglobin. - It is responsible for **binding oxygen** reversibly, which is myoglobin's primary function in muscle tissue. *Copper* - **Copper** is a component of several enzymes, such as **cytochrome c oxidase** and **superoxide dismutase**, but not myoglobin. - It plays a role in **electron transport** and connective tissue formation. *Selenium* - **Selenium** is an essential trace element that functions as a component of **glutathione peroxidase**, an antioxidant enzyme. - It is not found in the structure of myoglobin. *Zinc* - **Zinc** is a critical component of many enzymes, including **carbonic anhydrase** and **DNA polymerase**. - It is involved in **immune function** and wound healing, but not in oxygen transport by myoglobin.