Which of the following compounds is not formed with the involvement of glycine?
Which of the following is required in the synthesis of acetylcholine -
What is the respiratory quotient of carbohydrates?
Epinephrine increases free fatty acid levels by causing which of the following?
Energy source used by brain in later days of starvation is
Which of the following enzyme activity decreases in fasting?
Which of the following vitamins can be synthesized in the body in sufficient quantities to meet physiological needs?
Which metabolic pathway is least active during 12 days of fasting?
Pyridoxine is required in -
Pruritus [Itching] associated with Congenital Erythropoietic Porphyria is caused by deficiency of -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 41: Which of the following compounds is not formed with the involvement of glycine?
- A. Purines
- B. Glutathione
- C. Thyroxine (Correct Answer)
- D. Heme
Explanation: ***Thyroxine*** - **Thyroxine** (and other thyroid hormones) are derived from the amino acid **tyrosine**. - Their synthesis involves iodination and coupling reactions of tyrosine residues within the protein **thyroglobulin**. *Heme* - **Glycine** is a direct precursor for the initial step in **heme synthesis**. - It condenses with **succinyl CoA** to form α-amino-β-ketoadipate, which then decarboxylates to form δ-aminolevulinate (ALA). *Purines* - **Glycine** contributes part of its structure to the **purine ring**. - Specifically, the **nitrogen at position 7** and the **carbons at positions 4 and 5** of the purine ring are derived from glycine. *Glutathione* - **Glutathione** is a tripeptide composed of three amino acids: **glutamate**, **cysteine**, and **glycine**. - **Glycine** is the C-terminal amino acid of glutathione and is essential for its structure and function as an antioxidant.
Question 42: Which of the following is required in the synthesis of acetylcholine -
- A. Inositol
- B. Carnitine
- C. Glycine
- D. Choline (Correct Answer)
Explanation: ***Choline*** - **Choline** is a **precursor** to acetylcholine, providing the **choline moiety** for its synthesis. - The enzyme **choline acetyltransferase** combines choline with acetyl-CoA (which provides the acetyl group) to form acetylcholine. *Inositol* - **Inositol** is a sugar alcohol that plays a role in **cell signaling** and as a secondary messenger in various pathways. - It is not directly involved as a substrate in the synthesis of acetylcholine. *Carnitine* - **Carnitine** is essential for the **transport of fatty acids** into the mitochondria for beta-oxidation. - It does not participate in the enzymatic reactions that produce acetylcholine. *Glycine* - **Glycine** is an amino acid that functions as an **inhibitory neurotransmitter** in the central nervous system. - While it is a neurotransmitter, it is not a component or precursor for acetylcholine synthesis.
Question 43: What is the respiratory quotient of carbohydrates?
- A. 0.5
- B. 0.8
- C. 0.75
- D. 1 (Correct Answer)
Explanation: ***Option: 1 (Correct Answer)*** - The **respiratory quotient (RQ)** is the ratio of **carbon dioxide produced to oxygen consumed** during metabolism. - For carbohydrates, complete oxidation yields equal moles of CO2 and O2, resulting in an **RQ of 1.0**. - Example: C6H12O6 + 6O2 → 6CO2 + 6H2O, giving RQ = 6CO2/6O2 = 1.0 - This value reflects that carbohydrates are highly oxygenated molecules, requiring less external oxygen for their oxidation relative to the CO2 produced. *Option: 0.5* - An RQ of 0.5 is not observed for any major macronutrient during complete oxidation. - This value would imply significantly lower CO2 production relative to O2 consumption, which doesn't match any physiological substrate metabolism. *Option: 0.8* - An RQ of approximately 0.8 is characteristic of a **mixed diet** or the average value sometimes cited for **protein metabolism**. - Protein RQ typically ranges from 0.8-0.85, as proteins require more oxygen for their oxidation compared to the CO2 produced. - The exact RQ can vary depending on the specific amino acids being metabolized. *Option: 0.75* - An RQ around 0.7-0.75 may represent **fat-predominant metabolism** or a mixed diet with fats and carbohydrates. - Pure **fat metabolism** has an RQ of approximately **0.7**, as fats require substantial oxygen for oxidation due to their lower oxygen content relative to carbon and hydrogen. - Fats contain many C-H bonds and few C-O bonds, necessitating more oxygen for complete combustion.
Question 44: Epinephrine increases free fatty acid levels by causing which of the following?
- A. Increasing fatty acid synthesis
- B. Increasing lipolysis (Correct Answer)
- C. Increasing cholesterol catabolism
- D. None of the options
Explanation: ***Increasing lipolysis*** - Epinephrine activates **hormone-sensitive lipase** in adipose tissue through a **cAMP-dependent mechanism**, leading to the breakdown of stored triglycerides into free fatty acids and glycerol. - This process, known as **lipolysis**, directly increases the release of free fatty acids into the bloodstream. *Increased fatty acid synthesis* - **Fatty acid synthesis** is a process that builds fatty acids, which would decrease, not increase, free fatty acid levels in the blood. - Epinephrine's primary action is to mobilize energy reserves, which involves breaking down stored fats rather than synthesizing new ones. *Increasing cholesterol catabolism* - While cholesterol metabolism is important, epinephrine does not directly or significantly increase **cholesterol catabolism** as a primary mechanism for raising free fatty acid levels. - The catabolism of cholesterol primarily involves its conversion to bile acids and steroid hormones, which is distinct from fatty acid release. *None of the options* - This option is incorrect because increasing lipolysis is a direct and well-established mechanism by which epinephrine raises free fatty acid levels.
Question 45: Energy source used by brain in later days of starvation is
- A. Glucose
- B. Ketone bodies (Correct Answer)
- C. Glycogen
- D. Fatty acids
Explanation: ***Ketone bodies*** - During **prolonged starvation**, the liver produces **ketone bodies** (acetoacetate and β-hydroxybutyrate) from fatty acid breakdown. - The brain adapts to utilize these ketone bodies as a primary energy source, reducing its reliance on **glucose**. *Glucose* - While **glucose** is the primary energy source for the brain under normal conditions, its availability diminishes significantly during prolonged starvation. - The brain attempts to conserve glucose for essential functions by switching to alternative fuels. *Glycogen* - The brain stores very limited amounts of **glycogen**, which are rapidly depleted within minutes of glucose deprivation. - It is not a sustainable or significant energy source during extended periods of starvation. *Fatty acids* - **Fatty acids** cannot directly cross the **blood-brain barrier** to a significant extent, thus they are not a direct fuel source for brain cells. - They are, however, used by the liver to synthesize ketone bodies, which then serve as brain fuel.
Question 46: Which of the following enzyme activity decreases in fasting?
- A. Hormone sensitive lipase
- B. Glycogen phosphorylase
- C. Acetyl CoA Carboxylase
- D. Phosphofructokinase I (Correct Answer)
Explanation: ***Phosphofructokinase I*** - **Phosphofructokinase I (PFK-1)** activity **decreases** during fasting due to **decreased insulin-to-glucagon ratio**, which reduces **fructose-2,6-bisphosphate (F-2,6-BP)** levels, a powerful allosteric activator of PFK-1. - This reduction in activity slows down **glycolysis**, conserving glucose for critical tissues like the brain and redirecting metabolism toward **gluconeogenesis**. - **PFK-1 is the rate-limiting enzyme of glycolysis**, making its regulation particularly significant in the fasted state. *Hormone sensitive lipase* - **Hormone sensitive lipase (HSL)** activity **increases** during fasting due to elevated **glucagon** and **epinephrine** levels, which stimulate its phosphorylation via **protein kinase A (PKA)**. - This increased activity promotes the breakdown of stored **triglycerides** in adipose tissue, releasing **fatty acids** for β-oxidation and energy production. *Glycogen phosphorylase* - **Glycogen phosphorylase** activity **increases** during fasting, primarily stimulated by **glucagon** and **epinephrine**, leading to the breakdown of **glycogen** stores. - This enzyme is crucial for **glycogenolysis**, providing glucose to maintain blood sugar levels when dietary intake is absent. *Acetyl CoA Carboxylase* - **Acetyl CoA Carboxylase (ACC)** activity also **decreases** during fasting, as it is inhibited by **phosphorylation** mediated by **AMP-activated protein kinase (AMPK)** and **protein kinase A (PKA)**. - This reduction in activity inhibits **fatty acid synthesis**, shifting metabolism towards fatty acid **oxidation** for energy production. - **Note:** While ACC activity does decrease during fasting, **PFK-1** is considered the primary answer as it represents the key regulatory point for **glucose metabolism** (glycolysis vs. gluconeogenesis), which is the central metabolic shift during fasting.
Question 47: Which of the following vitamins can be synthesized in the body in sufficient quantities to meet physiological needs?
- A. Vitamin K
- B. Vitamin D (Correct Answer)
- C. Vitamin A
- D. Biotin
Explanation: ***Vitamin D*** - The skin synthesizes vitamin D (specifically **cholecalciferol**) upon exposure to **ultraviolet B (UVB) radiation** from sunlight. - This endogenous production can be sufficient to meet physiological needs under adequate sun exposure, making it conditionally non-essential in the diet. *Vitamin K* - While **intestinal bacteria synthesize some vitamin K (K2)**, it is generally not in sufficient quantities to meet all physiological needs, especially for blood clotting. - Dietary intake of **vitamin K1 (phylloquinone)** from leafy green vegetables is critical. *Vitamin A* - **Vitamin A (retinol)** is obtained primarily from the diet, either directly from animal sources or from carotenoid precursors (like **beta-carotene**) in plants. - The body cannot synthesize vitamin A de novo; it relies on dietary intake and conversion from precursors. *Biotin* - Although the **gut microbiota can synthesize biotin**, the amount produced is generally considered insufficient to meet the body's requirements. - Therefore, biotin is primarily obtained through dietary intake, functioning as a coenzyme in various metabolic reactions.
Question 48: Which metabolic pathway is least active during 12 days of fasting?
- A. Gluconeogenesis
- B. Glycogenolysis (Correct Answer)
- C. Ketogenesis
- D. Lipolysis
Explanation: ***Correct: Glycogenolysis*** - **Glycogenolysis**, the breakdown of glycogen stores, is very active during the **initial hours of fasting** (first 24-48 hours) to maintain blood glucose levels. - However, after **12 days of fasting**, liver and muscle **glycogen stores are completely depleted**, making this pathway **essentially inactive** or the least active of all the metabolic pathways. - Once glycogen is exhausted, this pathway cannot contribute further to energy metabolism. *Incorrect: Gluconeogenesis* - This pathway becomes **increasingly active** during prolonged fasting to **synthesize new glucose** from non-carbohydrate precursors (amino acids, lactate, glycerol). - Essential for maintaining blood glucose for **glucose-dependent tissues** like red blood cells and parts of the brain that haven't fully adapted to ketones. - Remains a **crucial and active pathway** throughout prolonged fasting. *Incorrect: Ketogenesis* - **Ketogenesis** is **highly active** during prolonged fasting, producing **ketone bodies** (acetoacetate, β-hydroxybutyrate) from fatty acids in the liver. - Provides the **primary alternative fuel** for the brain (up to 70% of brain energy needs) and other tissues. - This is a **key metabolic adaptation** to preserve protein and glucose during starvation. *Incorrect: Lipolysis* - **Lipolysis** (breakdown of triglycerides into fatty acids and glycerol) is **highly active** during fasting to mobilize stored energy. - Provides **fatty acids** for direct oxidation by most tissues and **glycerol** as a gluconeogenic substrate. - A **fundamental process** for energy supply during nutrient deprivation.
Question 49: Pyridoxine is required in -
- A. Glycolysis
- B. TCA cycle
- C. Glycogenesis
- D. Transamination (Correct Answer)
Explanation: ***Transamination*** - **Pyridoxal phosphate (PLP)**, the active form of pyridoxine (vitamin B6), is an essential **coenzyme for aminotransferases (transaminases)** - Transamination reactions involve the transfer of an **amino group** from an amino acid to a keto acid, which is crucial for amino acid metabolism - This is the classic biochemical function of vitamin B6 and a frequently tested concept *Glycolysis* - Glycolysis is a metabolic pathway that breaks down glucose into pyruvate - Key cofactors for glycolysis include **NAD+ and ATP**, not vitamin B6 - Does not require pyridoxine as a coenzyme *TCA cycle* - The **TCA cycle (Krebs cycle)** is a central metabolic pathway for energy production - Uses enzymes that require cofactors such as **NAD+, FAD, and Coenzyme A** (derived from pantothenic acid) - Pyridoxine is not directly involved as a coenzyme in TCA cycle reactions *Glycogenesis* - Glycogenesis is the process of synthesizing **glycogen from glucose** - Primarily involves enzymes like **glycogen synthase** and **branching enzyme** - Requires **UTP and glucose-1-phosphate**, not pyridoxine
Question 50: Pruritus [Itching] associated with Congenital Erythropoietic Porphyria is caused by deficiency of -
- A. Uroporphyrinogen - III synthase (Correct Answer)
- B. Uroporphyrinogen - I synthase
- C. 5-ALA dehydratase
- D. HMB synthase
Explanation: ***Uroporphyrinogen - III synthase*** - Congenital Erythropoietic Porphyria (CEP) is caused by a **deficiency of uroporphyrinogen III synthase**, leading to the accumulation of uroporphyrinogen I and coproporphyrinogen I. - These accumulated **Type I porphyrinogens** are non-functional in heme synthesis and are highly **photoreactive**, causing the characteristic photosensitivity and skin symptoms, including intense pruritus. *5-ALA dehydratase* - Deficiency of **5-ALA dehydratase** (also known as porphobilinogen synthase) is associated with **ALA dehydratase deficiency porphyria (ADP)**, a very rare acute hepatic porphyria. - Symptoms primarily involve **neurovisceral attacks** and do not typically include pruritus or photosensitivity. *Uroporphyrinogen - I synthase* - **Uroporphyrinogen I synthase** is an outdated and incorrect term; the correct enzyme in the heme synthesis pathway is **hydroxymethylbilane synthase (HMB synthase)** or **porphobilinogen deaminase (PBG deaminase)**, which synthesizes HMB. - Deficiency in HMB synthase leads to **acute intermittent porphyria (AIP)**, characterized by acute neurological attacks, not severe pruritus. *HMB synthase* - **HMB synthase** (hydroxymethylbilane synthase), also known as **porphobilinogen deaminase (PBG deaminase)**, is deficient in **acute intermittent porphyria (AIP)**. - AIP is marked by intermittent neurological dysfunction and abdominal pain, with **no significant photosensitivity or pruritus**.