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 -
Which fat-soluble vitamin is most classically known for its steroid hormone-like action through nuclear receptors?
Which of the following elements have antioxidant properties?
In the context of energy metabolism, which coenzyme is niacin a precursor to?
Which coenzyme is not required in the formation of glutamate?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 41: 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 42: 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 43: 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 44: 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 45: 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 46: 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**.
Question 47: Which fat-soluble vitamin is most classically known for its steroid hormone-like action through nuclear receptors?
- A. Vitamin K
- B. Vitamin D (Correct Answer)
- C. Vitamin A
- D. Vitamin E
Explanation: ***Correct Answer: Vitamin D*** - **Vitamin D** (specifically its active form, **calcitriol** or **1,25-dihydroxyvitamin D₃**) is the **most classically recognized** fat-soluble vitamin that functions as a **steroid hormone** - It binds to the **vitamin D receptor (VDR)**, which is a member of the **nuclear receptor superfamily** - This VDR-calcitriol complex acts as a transcription factor, regulating gene expression involved in **calcium and phosphate homeostasis**, bone metabolism, skeletal development, and immune function - The mechanism is analogous to classic steroid hormones like cortisol, estrogen, and testosterone *Incorrect: Vitamin A* - **Vitamin A** (as **retinoic acid**) also interacts with nuclear receptors (**retinoic acid receptors - RARs** and **retinoid X receptors - RXRs**) to regulate gene transcription - However, Vitamin A is **most classically associated** with vision (rhodopsin in retinal photoreceptors), epithelial cell differentiation, embryonic development, and immune function - While it does have nuclear receptor-mediated actions, **Vitamin D is more prominently described** as having steroid hormone-like activity in standard medical education *Incorrect: Vitamin K* - **Vitamin K** functions primarily as a **cofactor for γ-glutamyl carboxylase**, an enzyme that catalyzes post-translational modification of glutamate residues to γ-carboxyglutamate (Gla) - Essential for the synthesis of **clotting factors** (II, VII, IX, X, protein C, protein S) and bone proteins (osteocalcin) - Does **not** act through nuclear receptors or function as a steroid hormone *Incorrect: Vitamin E* - **Vitamin E** (α-tocopherol) is a powerful **lipid-soluble antioxidant** that protects cell membranes from oxidative damage by scavenging free radicals - Functions primarily through its **antioxidant properties**, not through nuclear receptor binding - Does **not** have steroid hormone-like actions
Question 48: Which of the following elements have antioxidant properties?
- A. Copper
- B. Zinc
- C. Selenium
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Selenium**, **copper**, and **zinc** all possess antioxidant properties, directly or indirectly, by being cofactors for various antioxidant enzymes or by directly scavenging free radicals. - These elements play crucial roles in maintaining **cellular redox balance** and protecting against **oxidative stress**. *Selenium* - It is a vital component of **glutathione peroxidase**, a key enzyme in the body's antioxidant defense system, which converts harmful **hydrogen peroxide** into water. - Selenium also contributes to the function of **thioredoxin reductases**, enzymes involved in regulating **redox signaling**. *Copper* - Copper is an essential cofactor for **superoxide dismutase (SOD1 and SOD3)**, an enzyme that catalyzes the dismutation of **superoxide radicals** into oxygen and hydrogen peroxide. - However, excessive copper can also act as a **pro-oxidant**, highlighting the importance of proper balance. *Zinc* - Zinc is another crucial cofactor for **superoxide dismutase (SOD1)** and is involved in protecting cells from **oxidative damage**. - It also stabilizes cell membranes, making them less susceptible to **oxidative damage**, and plays a role in regulating the expression of genes involved in **antioxidant defense**.
Question 49: In the context of energy metabolism, which coenzyme is niacin a precursor to?
- A. Thiamine pyrophosphate (TPP)
- B. NADP
- C. NAD (Correct Answer)
- D. Flavin adenine dinucleotide (FAD)
Explanation: ***NAD*** - Niacin (vitamin B3) is a direct precursor to **nicotinamide adenine dinucleotide (NAD/NAD+)**. - NAD is the crucial coenzyme in **energy metabolism**, primarily involved in **catabolic pathways** such as glycolysis, TCA cycle, and electron transport chain. - Functions as an **electron carrier** in redox reactions, accepting electrons during oxidation of fuel molecules. *Thiamine pyrophosphate (TPP)* - **Thiamine (vitamin B1)** is the precursor to TPP, not niacin. - TPP plays a vital role in **carbohydrate metabolism**, particularly in pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes. *NADP* - While niacin is also a precursor to **NADP/NADPH**, this coenzyme is primarily used in **anabolic (biosynthetic) pathways**, not energy metabolism. - NADP functions in reductive biosynthesis (fatty acid synthesis, cholesterol synthesis) and **oxidative stress protection** via the pentose phosphate pathway. - The question specifically asks about **energy metabolism**, making NAD the correct answer as it participates in catabolic, energy-producing reactions. *Flavin adenine dinucleotide (FAD)* - **Riboflavin (vitamin B2)** is the precursor to FAD, not niacin. - FAD is a coenzyme involved in various metabolic reactions, especially in the **TCA cycle** and **electron transport chain**, acting as an electron acceptor.
Question 50: Which coenzyme is not required in the formation of glutamate?
- A. None of the above
- B. Pyridoxal phosphate
- C. Thiamine pyrophosphate (Correct Answer)
- D. Niacin
Explanation: ***Thiamine pyrophosphate*** - **Thiamine pyrophosphate (TPP)** is a coenzyme derived from **vitamin B1** that is essential for reactions involving decarboxylation, such as those catalyzed by pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. - The formation of glutamate primarily involves transamination or reductive amination, which do not require TPP. *Pyridoxal phosphate* - **Pyridoxal phosphate (PLP)**, derived from **vitamin B6**, is a crucial coenzyme for **transamination reactions**, which are a major pathway for glutamate synthesis (e.g., from alpha-ketoglutarate). - It also plays a role in decarboxylation and deamination reactions of amino acids. *Niacin* - **Niacin (vitamin B3)** is a precursor for **NAD+** and **NADP+**, which are essential coenzymes in many metabolic pathways. - **NADPH**, derived from NADP+, is required as a reductant in the **reductive amination** of **alpha-ketoglutarate** to form glutamate, catalyzed by glutamate dehydrogenase. *None of the above* - This option is incorrect because **thiamine pyrophosphate** is indeed not required for the formation of glutamate. - The other two coenzymes, **pyridoxal phosphate** and **niacin (as NAD(P)H)**, are involved in glutamate synthesis.