Which of the following is a plasma protein involved in blood clotting?
Which of the following statements BEST describes the net ATP production in glycolysis?
Which of the following substances does not inhibit glycolysis?
Which tissue cannot convert glucose 6-phosphate to free glucose due to lack of glucose-6-phosphatase?
Mutation in GLUT-2 causes which syndrome?
Which of the following is monoenoic acid ?
Which of the following fatty acids has the maximum number of carbon atoms?
Chylomicron remnants are associated with ?
Which of the following statements is true regarding medium chain fatty acids?
In which condition does serum appear milky white?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 141: Which of the following is a plasma protein involved in blood clotting?
- A. Fibrinogen (Correct Answer)
- B. Lactate dehydrogenase (LDH)
- C. Aspartate aminotransferase (SGOT)
- D. Alanine aminotransferase (SGPT)
Explanation: ***Fibrinogen*** - **Fibrinogen** is a crucial plasma protein that is converted into **fibrin** during the coagulation cascade. - **Fibrin** then forms a meshwork, which is the structural basis of a **blood clot**. *Lactate dehydrogenase (LDH)* - **LDH** is an enzyme found in many tissues throughout the body and is involved in **cellular metabolism**, specifically the conversion of pyruvate to lactate. - Elevated levels of **LDH** can indicate tissue damage or disease but are not directly involved in blood clotting. *Aspartate aminotransferase (SGOT)* - **SGOT** (now commonly referred to as **AST**) is an enzyme primarily found in the **liver, heart, skeletal muscle, kidneys, brain, and red blood cells**. - High levels of **AST** are often indicative of **liver damage** or other organ injury, but it does not play a direct role in blood coagulation. *Alanine aminotransferase (SGPT)* - **SGPT** (now commonly referred to as **ALT**) is an enzyme predominantly found in the **liver**. - Elevated **ALT** levels are a sensitive marker for **liver cell damage** but are not involved in the blood clotting process.
Question 142: Which of the following statements BEST describes the net ATP production in glycolysis?
- A. Glycolysis produces 2 molecules of pyruvate
- B. Glycolysis produces a net gain of 2 ATP per glucose molecule (Correct Answer)
- C. Hexokinase consumes ATP during glycolysis
- D. Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules
Explanation: ***Glycolysis produces a net gain of 2 ATP per glucose molecule*** - In the initial "investment" phase of glycolysis, **2 ATP molecules are consumed** to phosphorylate glucose. - In the subsequent "payoff" phase, **4 ATP molecules are produced** through substrate-level phosphorylation, resulting in a net gain of 2 ATP. *Glycolysis produces 2 molecules of pyruvate* - While glycolysis does produce **2 molecules of pyruvate** from one glucose molecule, this statement describes the end product of the pathway, not the net ATP production. - Pyruvate is a crucial product that can be further metabolized in aerobic or anaerobic conditions, but it does not directly represent the energy yield in terms of ATP. *Hexokinase consumes ATP during glycolysis* - **Hexokinase** is indeed the enzyme that catalyzes the first ATP-consuming step in glycolysis, phosphorylating glucose to glucose-6-phosphate. - However, this statement describes only one aspect of ATP utilization within the pathway and does not account for the total ATP produced or the overall net gain. *Aldolase catalyzes the conversion of fructose-1,6-bisphosphate into two three-carbon molecules* - **Aldolase** is a key enzyme in glycolysis responsible for cleaving **fructose-1,6-bisphosphate** into dihydroxyacetone phosphate and glyceraldehyde-3-phosphate. - This step is part of the preparatory phase of glycolysis but does not directly describe the net ATP production.
Question 143: Which of the following substances does not inhibit glycolysis?
- A. Fluoride
- B. Arsenite
- C. Iodoacetate
- D. Fluoroacetate (Correct Answer)
Explanation: ***Fluoroacetate*** - **Fluoroacetate** is not a direct inhibitor of glycolysis. Instead, it is metabolized to **fluorocitrate**, which then acts as an inhibitor of **aconitase** in the **Krebs cycle (TCA cycle)**, thereby affecting cellular respiration at a later stage. - Its primary role in metabolic inhibition is within the **mitochondria**, impacting energy production via the TCA cycle rather than the glycolytic pathway. *Fluoride* - **Fluoride** is a known inhibitor of **enolase**, an enzyme in the penultimate step of glycolysis. - It forms a complex with **magnesium** and **phosphate** to block the active site of enolase, preventing the conversion of 2-phosphoglycerate to phosphoenolpyruvate. *Arsenite* - **Arsenite** inhibits glycolysis by targeting enzymes containing **sulfhydryl (–SH) groups**, particularly **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**, a critical enzyme in the glycolytic pathway. - It also inhibits the **pyruvate dehydrogenase complex** (linking glycolysis to the TCA cycle) and TCA cycle enzymes like **α-ketoglutarate dehydrogenase**, thereby affecting multiple stages of cellular respiration. *Iodoacetate* - **Iodoacetate** is a potent inhibitor of the enzyme **glyceraldehyde-3-phosphate dehydrogenase (GAPDH)**. - It specifically alkylates the **cysteine residue** at the active site of GAPDH, preventing the conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate, thereby blocking glycolysis.
Question 144: Which tissue cannot convert glucose 6-phosphate to free glucose due to lack of glucose-6-phosphatase?
- A. Liver
- B. Kidney
- C. Adipose tissue
- D. Muscle (Correct Answer)
Explanation: ***Muscle*** - Muscle tissue lacks the enzyme **glucose-6-phosphatase**, which is essential for hydrolyzing glucose 6-phosphate back to **free glucose**. - Therefore, glucose 6-phosphate in muscle is primarily used for **glycolysis** (energy production) or stored as glycogen for local use. *Liver* - The liver contains **glucose-6-phosphatase**, allowing it to convert **glucose 6-phosphate** to **free glucose**. - This capability is crucial for maintaining **blood glucose homeostasis** and releasing glucose into circulation. *Adipose tissue* - Adipose tissue, like muscle, **lacks glucose-6-phosphatase** and cannot convert glucose 6-phosphate back to free glucose. - Glucose 6-phosphate in adipose tissue is primarily channeled into **fatty acid synthesis** and storage. *Kidney* - The kidney, particularly the renal cortex, possesses **glucose-6-phosphatase** and can convert glucose 6-phosphate to **free glucose**. - This contributes to **gluconeogenesis** and release of glucose into the blood, especially during fasting.
Question 145: Mutation in GLUT-2 causes which syndrome?
- A. Dandy walker syndrome
- B. Beckwith-Wiedemann syndrome
- C. Menke's disease
- D. Fanconi-Bickel syndrome (Correct Answer)
Explanation: ***Fanconi-Bickel syndrome*** - This syndrome is caused by a **mutation in the GLUT-2 gene**, leading to dysfunctional glucose transport in the liver, kidneys, and intestines. - Key features include **hepatorenal glycogen accumulation**, **renal tubulopathy** (Fanconi syndrome), and **impaired glucose and galactose utilization**. *Dandy-Walker syndrome* - This is a **congenital brain malformation** involving the cerebellum and fourth ventricle. - It is often associated with hydrocephalus, but not directly linked to glucose transporter defects. *Beckwith-Wiedemann syndrome* - This is an **overgrowth disorder** characterized by a high risk of childhood cancer and congenital anomalies. - It is primarily caused by genetic abnormalities on **chromosome 11p15.5** and is unrelated to GLUT-2 mutations. *Menke's disease* - This is a rare X-linked recessive disorder of **copper metabolism**, leading to severe neurological degeneration. - It results from mutations in the **ATP7A gene**, which encodes a copper-transporting ATPase.
Question 146: Which of the following is monoenoic acid ?
- A. Linoleic acid
- B. Oleic acid (Correct Answer)
- C. Linolenic acid
- D. Arachidonic acid
Explanation: ***Oleic acid*** - **Oleic acid** is a **monounsaturated fatty acid** (MUFA), meaning it has **one double bond** in its hydrocarbon chain. - Its presence in many natural fats and oils makes it a significant component of the human diet. *Arachidonic acid* - **Arachidonic acid** is a **polyunsaturated fatty acid** (PUFA) containing **four double bonds**. - It is a precursor for **eicosanoids**, including prostaglandins and leukotrienes, involved in inflammation and other physiological processes. *Linoleic acid* - **Linoleic acid** is an **essential omega-6 polyunsaturated fatty acid** with **two double bonds**. - It is crucial for human health and serves as a precursor for other fatty acids like arachidonic acid. *Linolenic acid* - **Linolenic acid** refers to two essential fatty acids: **alpha-linolenic acid (ALA)**, an omega-3 fatty acid with **three double bonds**, and **gamma-linolenic acid (GLA)**, an omega-6 fatty acid also with three double bonds. - Both are **polyunsaturated fatty acids** with multiple double bonds.
Question 147: Which of the following fatty acids has the maximum number of carbon atoms?
- A. Oleic acid
- B. Linolenic acid
- C. Arachidonic acid
- D. Cervonic acid (Correct Answer)
Explanation: **Cervonic acid** - **Cervonic acid**, also known as **docosahexaenoic acid (DHA)**, is a long-chain omega-3 fatty acid with **22 carbon atoms** and 6 double bonds (22:6). - It is a primary structural component of the brain and retina and is the longest fatty acid among the options provided. *Oleic acid* - **Oleic acid** is a monounsaturated fatty acid with **18 carbon atoms** and one double bond (18:1). - It is a common fatty acid found in many animal fats and vegetable oils, but it has fewer carbon atoms than cervonic acid. *Linolenic acid* - **Linolenic acid** refers to two essential fatty acids: alpha-linolenic acid (ALA) and gamma-linolenic acid (GLA). Both have **18 carbon atoms**. - Alpha-linolenic acid (ALA) is an omega-3 fatty acid with 3 double bonds (18:3), while gamma-linolenic acid (GLA) is an omega-6 fatty acid with 3 double bonds (18:3), neither of which has more carbon atoms than cervonic acid. *Arachidonic acid* - **Arachidonic acid** is an omega-6 fatty acid with **20 carbon atoms** and four double bonds (20:4). - It is a precursor to eicosanoids and is longer than oleic and linolenic acids but shorter than cervonic acid.
Question 148: Chylomicron remnants are associated with ?
- A. Apo-C
- B. Apo-A
- C. Apo-E (Correct Answer)
- D. Apo-B100
Explanation: ***Apo-E*** - **Apolipoprotein E (Apo-E)** is a crucial apolipoprotein on the surface of chylomicron remnants, acting as a **ligand for the LDL receptor-related protein 1 (LRP1)** in the liver. - This binding facilitates the **hepatic uptake and clearance** of chylomicron remnants from circulation. *Apo-A* - **Apo-AI** is the primary apolipoprotein of **HDL** and plays a key role in reverse cholesterol transport by activating **lecithin-cholesterol acyltransferase (LCAT)**. - While chylomicrons *acquire* some Apo-AI from HDL, it is not the primary apolipoprotein defining their remnants' hepatic clearance. *Apo-C* - **Apo-CII** is a vital activator of **lipoprotein lipase (LPL)**, which metabolizes triglycerides in chylomicrons and VLDL. - **Apo-CIII** inhibits LPL and hinders receptor-mediated uptake, but **Apo-E** is the key for remnant recognition and uptake, not Apo-C in general. *Apo-B100* - **Apo-B100** is the main structural apolipoprotein of **LDL** and **VLDL**, serving as the ligand for the LDL receptor, mediating their hepatic uptake. - While chylomicrons have **Apo-B48**, which is a truncated form of Apo-B100, Apo-B100 itself is not found on chylomicron remnants.
Question 149: Which of the following statements is true regarding medium chain fatty acids?
- A. All of the options are true (Correct Answer)
- B. Do not require pancreatic lipase for digestion
- C. Absorb directly into portal circulation
- D. Are less likely to be deposited in adipose tissue compared to long-chain fatty acids
Explanation: ***All of the options are true*** - This option is correct because medium-chain fatty acids (MCFAs) possess unique metabolic properties that differentiate them from long-chain fatty acids (LCFAs), making all listed statements accurate. - Their shorter chain length allows for distinct digestion, absorption, and metabolic fates, which are beneficial in various clinical contexts. *Do not require pancreatic lipase for digestion* - MCFAs have **shorter carbon chains** (typically 6-12 carbons) and are more hydrophilic than LCFAs. - This property allows them to be digested by **lingual and gastric lipases** to a greater extent, reducing the reliance on pancreatic lipase. *Absorb directly into portal circulation* - Unlike LCFAs, which are re-esterified into triglycerides, packaged into **chylomicrons**, and absorbed into the lymphatic system, MCFAs are absorbed directly into the **portal vein**. - This bypasses the lymphatic system and directly transports them to the liver, making them a rapid energy source. *Are less likely to be deposited in adipose tissue compared to long-chain fatty acids* - MCFAs are **rapidly oxidized** in the liver for energy via beta-oxidation and are less likely to be stored as triglycerides in adipose tissue. - They are also not efficiently utilized for the synthesis of complex lipids or stored fat due to their unique metabolic pathway and preference for oxidation.
Question 150: In which condition does serum appear milky white?
- A. Increased LDL
- B. Increased HDL
- C. Increased VLDL
- D. Increased Chylomicrons (Correct Answer)
Explanation: ***Increased Chylomicrons*** - **Chylomicrons** are the largest lipoprotein particles (75-1200 nm) with the highest **triglyceride content (85-95%)**, giving serum a characteristic **milky white** or "creamy" appearance - This intense milky appearance occurs after **fatty meals** (postprandial lipemia) or in **Type I and V hyperlipidemias** (familial chylomicronemia syndrome) - The **light scattering** by these large particles makes the serum completely opaque, distinguishing it from other lipid abnormalities - Classic clinical finding: **"cream layer" forms on top** when lipemic serum stands overnight in refrigerator *Increased LDL* - Elevated **Low-Density Lipoprotein (LDL)** produces **clear to slightly hazy** serum, never milky white - LDL particles are much smaller (18-25 nm) than chylomicrons and contain primarily **cholesterol**, not triglycerides - High LDL is a cardiovascular risk factor but does not cause visible lipemia *Increased HDL* - **High-Density Lipoprotein (HDL)** elevation results in **clear serum** - HDL particles are the smallest (5-12 nm) and densest lipoproteins - High HDL is protective and causes no turbidity *Increased VLDL* - **Very Low-Density Lipoprotein (VLDL)** elevation can cause **turbid or hazy** serum in severe hypertriglyceridemia, but typically less intensely milky than chylomicrons - VLDL particles are smaller (30-80 nm) than chylomicrons with lower triglyceride content (50-65%) - In Type IV hyperlipidemia (isolated VLDL elevation), serum appears uniformly turbid without cream layer formation - The most dramatic "milky white" appearance is specifically associated with **chylomicronemia**