Lipid Metabolism — MCQs

Lipid Metabolism Indian Medical PG Practice Questions and MCQs

Question 671: HDL is called good cholesterol because -

A. Removes cholesterol from peripheral tissues (Correct Answer)
B. Increases cholesterol delivery to peripheral tissues
C. Stimulates cholesterol synthesis in the liver
D. Activates enzymes that break down triglycerides

Explanation: ***Removes cholesterol from peripheral tissues*** - **High-density lipoprotein (HDL)** is known as "good cholesterol" due to its role in **reverse cholesterol transport**, a process where it collects excess cholesterol from peripheral cells and tissues. - This action helps to prevent the accumulation of cholesterol in arteries, thereby reducing the risk of **atherosclerosis** and cardiovascular disease. - HDL then transports this cholesterol to the liver for excretion via bile, completing the protective cycle. *Increases cholesterol delivery to peripheral tissues* - This is actually the opposite of HDL's function and describes the role of **LDL (low-density lipoprotein)**, which is considered "bad cholesterol." - LDL delivers cholesterol to peripheral tissues, and excess LDL can lead to **atherosclerotic plaque formation**. *Stimulates cholesterol synthesis in the liver* - HDL does not directly stimulate cholesterol synthesis in the liver; rather, its role is primarily in **cholesterol efflux** from cells and transport. - The liver's cholesterol synthesis is regulated by various factors, including dietary intake and cellular cholesterol levels via the **SREBP pathway**, but HDL does not upregulate hepatic cholesterol synthesis. *Activates enzymes that break down triglycerides* - While HDL does activate **LCAT (lecithin-cholesterol acyltransferase)** for cholesterol esterification, its primary "good" function is not the breakdown of triglycerides. - **Lipoprotein lipase (LPL)** is the primary enzyme responsible for triglyceride breakdown in lipoproteins like VLDL and chylomicrons.

Question 672: Which of the following statements about adiponectin is incorrect?

A. Secreted by adipose tissue
B. Increases FFA oxidation
C. Lowers glucose
D. Positive Correlation with BMI (Correct Answer)

Explanation: ***Positive Correlation with BMI (INCORRECT STATEMENT)*** - Adiponectin levels are **inversely correlated with BMI**, NOT positively correlated; as BMI increases, adiponectin levels generally decrease. - This inverse relationship is significant because lower adiponectin levels are associated with increased insulin resistance and **metabolic syndrome**. - This statement is **false**, making it the correct answer to this question. *Secreted by adipose tissue (Correct statement)* - Adiponectin is a **hormone primarily secreted by adipocytes** (fat cells). - It plays a crucial role in regulating glucose and lipid metabolism, and its secretion is altered in conditions like obesity. - This statement is **true**. *Lowers glucose (Correct statement)* - Adiponectin **enhances insulin sensitivity** in peripheral tissues like skeletal muscle and liver, leading to increased glucose uptake and utilization. - This action helps to **lower blood glucose levels** and improve glycemic control. - This statement is **true**. *Increases FFA oxidation (Correct statement)* - Adiponectin **promotes fatty acid oxidation** in muscle and liver, reducing intracellular lipid accumulation. - By increasing fatty acid burning, it helps to **decrease circulating free fatty acid (FFA) levels**, which can contribute to insulin resistance if elevated. - This statement is **true**.

Question 673: What is the primary receptor for High-Density Lipoprotein (HDL) in cholesterol metabolism?

A. SR-BI (Correct Answer)
B. LDLR
C. HDLR
D. SR-82

Explanation: ***SR-BI*** - **Scavenger Receptor class B type 1 (SR-BI)** is the primary receptor responsible for selective uptake of **cholesteryl esters** from HDL into cells, particularly the liver and steroidogenic tissues. - Unlike other lipoprotein receptors, SR-BI mediates the **selective transfer** of cholesterol without internalizing the entire HDL particle. *LDLR* - The **Low-Density Lipoprotein Receptor (LDLR)** is the primary receptor for **LDL** and very low-density lipoprotein (VLDL) remnants, mediating their endocytosis and degradation. - While it plays a crucial role in cholesterol metabolism, its main function is related to the uptake of **LDL cholesterol**, not HDL. *HDLR* - **HDLR** is not a recognized receptor in cholesterol metabolism. - This term may be a distracter created by combining HDL with the common receptor nomenclature. *SR-82* - **SR-82** is not a recognized receptor involved in cholesterol metabolism. - Similar to HDLR, this is a distracter term.

Question 674: Which of the following stimulates Acetyl CoA Carboxylase?

A. Starvation
B. Glucagon
C. Citrate (Correct Answer)
D. None of the options

Explanation: ***Citrate*** - **Citrate** is an allosteric activator of **Acetyl-CoA Carboxylase (ACC)**, indicating abundant energy and precursor availability for fatty acid synthesis. - This activation promotes the conversion of **Acetyl-CoA** to **Malonyl-CoA**, the committed step in **fatty acid synthesis**. *Starvation* - **Starvation** leads to energy deficit, which generally **inhibits** anabolic processes like fatty acid synthesis. - In this state, enzymes involved in anabolic pathways are often downregulated or inhibited to conserve energy. *Glucagon* - **Glucagon** is a hormone that signals low blood glucose and promotes catabolic processes such as **glycogenolysis** and **gluconeogenesis**. - It **inhibits** fatty acid synthesis by phosphorylating and inactivating **Acetyl-CoA Carboxylase**, thus opposing citrate's activating effect. *None of the options* - **Citrate** is a known stimulator of Acetyl CoA Carboxylase. - This option is incorrect because there is a correct answer among the choices.

Question 675: What is the role of colipase in fat digestion?

A. Encoded by the gene CLPS
B. Assists pancreatic lipase in fat digestion (Correct Answer)
C. Is secreted in an inactive form
D. Is secreted by pancreatic cells

Explanation: ***Assists pancreatic lipase in fat digestion*** - Colipase **binds to pancreatic lipase** and the **lipid-water interface** of the fat droplet, providing a conformational change that enables lipase to access and hydrolyze triglycerides. - It also prevents bile salts from inactivating pancreatic lipase, ensuring efficient **fat emulsification and digestion**. *Is secreted in an inactive form* - Colipase is secreted as **procolipase** by the pancreas, which is then activated by **trypsin** in the duodenum. - While correct, this option describes its activation rather than its primary role in fat digestion. *Encoded by the gene CLPS* - The gene **CLPS** indeed encodes for colipase, but this is a genetic detail rather than its functional role in the digestive process. - Knowledge of the encoding gene is not directly relevant to understanding its biochemical function in fat digestion. *Is secreted by pancreatic cells* - Colipase is indeed synthesized and secreted by the **pancreas** into the small intestine. - This statement is true but describes the **origin** of colipase, not its specific functional role in fat digestion.

Question 676: 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 677: Rate limiting enzyme in bile acid synthesis?

A. Desmolase
B. 21α-hydroxylase
C. 7α-hydroxylase (Correct Answer)
D. 12α-hydroxylase

Explanation: ***7α-hydroxylase*** - This enzyme, specifically **cholesterol 7α-hydroxylase**, catalyzes the first and rate-limiting step in the classic pathway of **bile acid synthesis**, converting cholesterol to 7α-hydroxycholesterol. - Its activity is tightly regulated, primarily by the availability of cholesterol and feedback inhibition by bile acids, making it a key control point. *Desmolase* - **Cholesterol desmolase** (CYP11A1) is the rate-limiting enzyme in **steroid hormone synthesis** in the adrenal glands, converting cholesterol to pregnenolone. - It is not involved in the committed steps of bile acid synthesis from cholesterol. *21α-hydroxylase* - **21α-hydroxylase** (CYP21A2) is crucial in the synthesis of **cortisol and aldosterone** from progesterone and 17-hydroxyprogesterone, respectively. - Deficiency in this enzyme is the most common cause of **congenital adrenal hyperplasia**, but it has no direct role in bile acid synthesis. *12α-hydroxylase* - **12α-hydroxylase** (CYP8B1) is an enzyme involved in the later steps of bile acid synthesis, specifically in the formation of **cholic acid** from 7α-hydroxy-4-cholesten-3-one. - While essential for synthesizing primary bile acids, it is not the *rate-limiting enzyme* for the overall pathway; 7α-hydroxylase holds that distinction.

Question 678: Bile acids consist of all of the following except -

A. Lithocholic acid
B. Deoxycholic acid
C. Bilirubin (Correct Answer)
D. Chenodeoxycholic acid

Explanation: ***Bilirubin*** - **Bilirubin** is a pigment formed from the breakdown of **heme**, not a bile acid. - It is excreted in bile but does not aid in **lipid digestion** or **absorption**. *Lithocholic acid* - **Lithocholic acid** is a **secondary bile acid** formed in the colon by bacterial dehydroxylation of chenodeoxycholic acid. - It is still considered a bile acid, despite its secondary nature. *Deoxycholic acid* - **Deoxycholic acid** is a **secondary bile acid** formed by bacterial action on cholic acid in the colon. - Like other bile acids, it plays a role in **fat digestion** and **absorption**. *Chenodeoxycholic acid* - **Chenodeoxycholic acid** is a **primary bile acid** synthesized in the liver from cholesterol. - It is one of the main bile acids directly involved in **emulsifying dietary fats**.

Question 679: Which of the following is NOT an enzyme involved in fatty acid synthesis?

A. Ketoacyl synthase
B. Enoyl reductase
C. Acetyl Co-A carboxylase
D. Acetoacetyl-CoA (Correct Answer)

Explanation: ***Acetoacetyl-CoA*** - **Acetoacetyl-CoA** is an intermediate compound, not an enzyme. - It is a **ketone body precursor** and also an intermediate in fatty acid synthesis and degradation. - It serves as a **substrate** for various enzymes but does not catalyze any reaction itself. *Acetyl Co-A carboxylase* - **Acetyl Co-A carboxylase** is the key regulatory enzyme in fatty acid synthesis, catalyzing the **carboxylation of acetyl-CoA** to form malonyl-CoA. - This reaction is the **rate-limiting step** and the **committed step** in fatty acid synthesis. - It requires **biotin** as a cofactor. *Ketoacyl synthase* - **Ketoacyl synthase** (beta-ketoacyl-ACP synthase) is a core catalytic domain of the fatty acid synthase complex. - It catalyzes the **condensation reaction** between an acyl group and malonyl-ACP, releasing CO₂. - This forms a **beta-ketoacyl-ACP intermediate**. *Enoyl reductase* - **Enoyl reductase** (enoyl-ACP reductase) is an enzyme domain in the fatty acid synthase complex. - It catalyzes the **final reduction step**, converting trans-enoyl-ACP to saturated acyl-ACP. - This reaction uses **NADPH** as the reducing agent.

Question 680: How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?

A. 3 acetyl CoA
B. 16 Acetyl CoA
C. 6 acetyl CoA
D. 8 acetyl CoA (Correct Answer)

Explanation: ***8 acetyl CoA*** - Palmitic acid is a **16-carbon saturated fatty acid (C16:0)**. During β-oxidation, each cycle cleaves two carbons as **acetyl CoA**. - The formula for acetyl CoA produced is **n/2**, where n = number of carbons. For palmitic acid: 16/2 = **8 acetyl CoA molecules**. - Alternatively: Palmitic acid undergoes **7 cycles of β-oxidation** [(n/2) - 1 = 7], each producing 1 acetyl CoA (7 total), plus the final 2-carbon fragment forming the 8th acetyl CoA. *3 acetyl CoA* - This number is too low for a 16-carbon fatty acid. **Short-chain fatty acids** would produce fewer acetyl CoA molecules. - This value corresponds to β-oxidation of a **6-carbon fatty acid** (hexanoic acid), not palmitic acid. *6 acetyl CoA* - This number is also too low for a 16-carbon fatty acid. - This quantity would be produced from a **12-carbon fatty acid** (lauric acid), not palmitic acid. *16 Acetyl CoA* - This number is too high and would incorrectly imply that each carbon forms an acetyl CoA independently. - Sixteen acetyl CoA molecules would be produced from a **32-carbon fatty acid**, which is extremely rare in biological systems.

Practice by Chapter

Lipid Classification and Chemistry

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Fatty Acid Oxidation

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Ketone Body Metabolism

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Fatty Acid Synthesis

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Metabolism of Triacylglycerols

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Phospholipid Metabolism

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Cholesterol Metabolism and Biosynthesis

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Bile Acids and Bile Salts

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Lipoprotein Metabolism and Transport

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Dyslipidemias and Atherosclerosis

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Prostaglandins and Eicosanoids

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Fatty Liver and Lipotropic Factors

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