Lipid Metabolism — MCQs

Lipid Metabolism Indian Medical PG Practice Questions and MCQs

Question 671: 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 672: 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 673: Transport of lipids from the intestine to other tissues is by -

A. Chylomicrons (Correct Answer)
B. LDL
C. HDL
D. VLDL

Explanation: ***Chylomicrons*** - **Chylomicrons** are the **largest lipoprotein particles** that transport **dietary (exogenous) lipids** from the **intestine** to peripheral tissues - They are synthesized in **intestinal enterocytes** after fat absorption and enter the bloodstream via the **lymphatic system (thoracic duct)** - They carry **triglycerides (85-95%), cholesterol, phospholipids, and fat-soluble vitamins** (A, D, E, K) - **Apolipoprotein B-48** is the characteristic structural protein of chylomicrons - After delivering triglycerides to tissues (via lipoprotein lipase), chylomicron remnants are taken up by the **liver** *LDL (Low-Density Lipoprotein)* - LDL transports **cholesterol from the liver to peripheral tissues** (not from intestine) - It carries **endogenous cholesterol**, not dietary lipids from the intestine - Often called "**bad cholesterol**" due to its role in atherosclerosis - Contains **Apolipoprotein B-100** *HDL (High-Density Lipoprotein)* - HDL performs **reverse cholesterol transport** - moving excess cholesterol from peripheral tissues **back to the liver** - It does **not transport lipids from the intestine** to tissues - Called "**good cholesterol**" for its protective cardiovascular role - Contains **Apolipoprotein A-I and A-II** *VLDL (Very-Low-Density Lipoprotein)* - VLDL is synthesized in the **liver** (not intestine) and transports **endogenous triglycerides** to peripheral tissues - It carries lipids **from the liver**, not from the intestine - VLDL is converted to IDL and then LDL after losing triglycerides - Contains **Apolipoprotein B-100**

Question 674: Bile acids are synthesized from ?

A. Heme
B. Ribulose
C. Arachidonic acid
D. Cholesterol (Correct Answer)

Explanation: ***Cholesterol*** - **Bile acids** are derivatives of **cholesterol**, synthesized in the liver through a multi-step enzymatic pathway. - The conversion of cholesterol to bile acids is a primary mechanism for the excretion and transport of cholesterol from the body. *Heme* - **Heme** is a component of hemoglobin and myoglobin, primarily involved in oxygen transport and storage. - Its degradation product is **bilirubin**, which forms part of bile but is distinct from bile acids. *Ribulose* - **Ribulose** is a 5-carbon sugar, playing a key role in the **pentose phosphate pathway** and the **Calvin cycle** in photosynthesis. - It is not a precursor for bile acid synthesis. *Arachidonic acid* - **Arachidonic acid** is a polyunsaturated fatty acid that serves as a precursor for **eicosanoids** (prostaglandins, thromboxanes, and leukotrienes). - These molecules are involved in inflammation and immune responses but are unrelated to bile acid synthesis.

Question 675: Which protein does the domain of plasminogen resemble?

A. Fibrinogen (a clotting protein)
B. LDL receptor (a lipid metabolism protein)
C. Apolipoprotein (a) (a lipoprotein) (Correct Answer)
D. Prothrombin (a coagulation protein)

Explanation: ***Apolipoprotein (a) (a lipoprotein)*** - **Plasminogen** and **apolipoprotein (a)** share structural homology, specifically due to the presence of **kringle domains**. - This structural similarity suggests a potential for apolipoprotein (a) to **interfere with plasminogen’s fibrinolytic activity**, contributing to **atherosclerosis**. *Fibrinogen (a clotting protein)* - While plasmin acts on fibrinogen (and its derivative fibrin), its domain structure does not **resemble fibrinogen**. - **Fibrinogen** is a large, multi-domain glycoprotein crucial for **clot formation**, distinct from plasminogen's primarily **kringle-rich structure**. *LDL receptor (a lipid metabolism protein)* - The **LDL receptor** is involved in **cholesterol uptake** by cells and has structural features like ligand-binding repeats and epidermal growth factor (EGF) repeats. - Its domain structure is **not similar to plasminogen**, which is characterized by **kringle domains** and a protease domain. *Prothrombin (a coagulation protein)* - **Prothrombin** is a precursor to thrombin, featuring **gla domains**, kringle-like domains (though structurally distinct from plasminogen's), and a serine protease domain. - While both are involved in coagulation/fibrinolysis, their **overall domain arrangements and specific kringle structures differ** significantly.

Question 676: What primarily forms the core of chylomicrons?

A. Triglycerides and Cholesterol together
B. Triglycerides (Correct Answer)
C. Free fatty acids
D. Triglyceride, Cholesterol and Phospholipids

Explanation: ***Triglycerides*** - Chylomicrons are primarily responsible for transporting **dietary triglycerides** from the intestines to other tissues. - Their large core, composed mainly of **triglycerides**, allows efficient transport of these hydrophobic molecules. *Triglycerides and Cholesterol together* - While **cholesterol** is present in chylomicrons, it is less abundant than **triglycerides** and primarily exists as **cholesterol esters** in the core. - The core is not an equal mixture; **triglycerides** overwhelmingly dominate the volume. *Free fatty acids* - **Free fatty acids** are transported in the blood primarily bound to **albumin**, not within the core of chylomicrons. - Chylomicrons typically carry **esterified fatty acids** as part of triglycerides. *Triglyceride, Cholesterol and Phospholipids* - **Phospholipids** form the outer monolayer of the chylomicron, along with apoproteins, making them **amphipathic**. - They do not constitute a core component but rather the **surface interface** with the aqueous environment.

Question 677: 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 678: 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 679: 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 680: 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.

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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