Lipid Metabolism — MCQs

Lipid Metabolism Indian Medical PG Practice Questions and MCQs

Question 671: 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 672: 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 673: Apo B48 is synthesized in -

A. Liver
B. Kidney
C. Intestine (Correct Answer)
D. RBCs

Explanation: ***Intestine*** - **Apo B48** is a truncated form of apolipoprotein B-100, uniquely synthesized in the **intestine** through RNA editing. - It is a crucial structural component of **chylomicrons**, which are lipoprotein particles responsible for transporting exogenous dietary lipids from the intestine to other tissues. *Liver* - The liver primarily synthesizes **Apo B100**, which is a full-length apolipoprotein B and a major component of VLDL, IDL, and LDL. - It does not produce Apo B48. *Kidney* - The kidneys are involved in filtering waste products and regulating fluid balance, but they do not play a role in the synthesis of apolipoproteins like Apo B48. - Kidney cells are not equipped with the specific machinery for Apo B mRNA editing. *RBCs* - Red blood cells (RBCs) are primarily responsible for oxygen transport and lack a nucleus and most organelles, including those required for protein synthesis. - Therefore, RBCs cannot synthesize proteins such as Apo B48.

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: 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 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: 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.

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 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 680: 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.

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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