Lipid Metabolism — MCQs
On this page
The major carrier of cholesterol in plasma is:
More than 50% of polyunsaturated fatty acids are seen in all, except:
From which of the following cellular locations are ketone bodies synthesized?
Which lipid is primarily elevated in poorly controlled diabetes mellitus?
What is the primary apolipoprotein deficiency associated with broad beta disease (familial type III hyperlipoproteinemia)?
All are true about beta-oxidation except:
What is the major apolipoprotein of chylomicrons?
Which of the following is the MOST accurate statement regarding thromboxane A2?
Which of the following is most strongly associated with heart disease?
Lipid Metabolism Indian Medical PG Practice Questions and MCQs
Question 761: The major carrier of cholesterol in plasma is:
- A. Very-Low-Density Lipoprotein (VLDL)
- B. Low-Density Lipoprotein (LDL) (Correct Answer)
- C. Chylomicrons
- D. High-Density Lipoprotein (HDL)
Explanation: ***Low-Density Lipoprotein (LDL)*** - **LDL** is the **major carrier of cholesterol in plasma**, transporting approximately **60-70% of total plasma cholesterol**. - It is primarily responsible for delivering **cholesterol** from the liver to peripheral tissues for **membrane synthesis**, **steroid hormone production**, and other cellular functions. - LDL cholesterol levels are the primary target for cardiovascular risk assessment and management. *Very-Low-Density Lipoprotein (VLDL)* - **VLDL** primarily transports **triglycerides** (55-65% of its content) synthesized in the liver to peripheral tissues. - While it contains some cholesterol (~10-15%), its main function is **triglyceride delivery**, and it serves as a precursor to LDL in the circulation. *Chylomicrons* - **Chylomicrons** are responsible for transporting **dietary triglycerides** and **cholesterol** from the intestines to tissues. - They are the largest lipoproteins and primarily transport **exogenous (dietary) lipids**. - Cholesterol represents only 3-5% of chylomicron content. *High-Density Lipoprotein (HDL)* - **HDL** carries approximately **20-30% of plasma cholesterol** and plays a crucial role in **reverse cholesterol transport**. - It collects excess cholesterol from peripheral tissues and returns it to the liver for excretion. - While functionally important for cholesterol homeostasis (protective against atherosclerosis), it carries significantly less cholesterol than LDL.
Question 762: More than 50% of polyunsaturated fatty acids are seen in all, except:
- A. Canola oil (Correct Answer)
- B. Soybean oil
- C. Safflower oil
- D. Corn oil
Explanation: ***Canola oil*** - While canola oil is a source of **polyunsaturated fatty acids (PUFA)**, its total PUFA content typically ranges from 25-35%, which is not more than 50%. - It is particularly rich in **monounsaturated fatty acids (MUFA)**, primarily **oleic acid**, which can make up a higher percentage of its fat content. *Soybean oil* - Soybean oil is known for its high content of **polyunsaturated fatty acids (PUFA)**, particularly **linoleic acid (omega-6)** and **alpha-linolenic acid (omega-3)**. - Its total PUFA content commonly exceeds **50%**, making it a significant source of these essential fatty acids. *Safflower oil* - Safflower oil is exceptionally rich in **polyunsaturated fatty acids (PUFA)**, especially **linoleic acid (omega-6)**. - Depending on the variety, its linoleic acid content alone can be over **70%**, ensuring its total PUFA content is well over 50%. *Corn oil* - Corn oil is another common vegetable oil with a high proportion of **polyunsaturated fatty acids (PUFA)**, predominantly **linoleic acid**. - Its PUFA content typically ranges from **50-60%**, meeting the criterion of having more than 50% PUFA.
Question 763: From which of the following cellular locations are ketone bodies synthesized?
- A. Cytosol
- B. ER
- C. Peroxisomes
- D. Mitochondria (Correct Answer)
Explanation: ***Mitochondria*** - **Ketone bodies**, namely **acetoacetate** and **beta-hydroxybutyrate**, are primarily synthesized in the mitochondrial matrix of liver cells. - This process, known as **ketogenesis**, occurs when **acetyl-CoA** levels are high, typically due to increased fatty acid oxidation during fasting or uncontrolled diabetes. *Cytosol* - The **cytosol** is the site of many metabolic pathways, including **glycolysis** and the pentose phosphate pathway, but not ketone body synthesis. - While some steps of fatty acid synthesis occur in the cytosol, a distinct process from ketogenesis, ketone body formation happens in a separate compartment. *ER* - The **endoplasmic reticulum (ER)** is involved in protein synthesis and folding, lipid synthesis, and detoxification. - It does not play a direct role in the synthesis of ketone bodies. *Peroxisomes* - **Peroxisomes** are involved in processes like **beta-oxidation of very long-chain fatty acids** and the synthesis of plasmalogens. - While involved in lipid metabolism, they are not the primary site for the synthesis of ketone bodies.
Question 764: Which lipid is primarily elevated in poorly controlled diabetes mellitus?
- A. HDL
- B. Triglycerides (Correct Answer)
- C. Cholesterol
- D. VLDL
Explanation: ***Triglycerides*** - In poorly controlled **diabetes mellitus**, insulin deficiency or resistance leads to increased hepatic synthesis of **triglycerides** and impaired clearance from the bloodstream. - This often results in **hypertriglyceridemia**, a common dyslipidemia in diabetic patients, contributing to increased cardiovascular risk. *HDL* - **High-density lipoprotein (HDL)** levels are typically **decreased** in poorly controlled diabetes due to increased catabolism and reduced synthesis. - Low HDL is considered an independent risk factor for **atherosclerosis** and is a common finding in diabetic dyslipidemia. *VLDL* - While **Very Low-Density Lipoprotein (VLDL)** levels may be elevated in diabetes, this is primarily due to increased synthesis and secretion of **triglyceride-rich VLDL** particles from the liver. - Therefore, the elevation in **VLDL** is a consequence of the underlying **hypertriglyceridemia**. *Cholesterol* - **Total cholesterol** levels can be elevated in poorly controlled diabetes, but this is often a consequence of an increase in **LDL cholesterol** and **triglycerides**. - **Total cholesterol** itself is not the primary lipid that is directly elevated as a first-order effect of the metabolic derangement.
Question 765: What is the primary apolipoprotein deficiency associated with broad beta disease (familial type III hyperlipoproteinemia)?
- A. Apo A
- B. Apo B
- C. Apo C
- D. Apo E (Correct Answer)
Explanation: ***Apo E*** - **Familial type III hyperlipoproteinemia**, also known as broad beta disease or dysbetalipoproteinemia, is primarily caused by homozygosity for the **ApoE2 allele**. - ApoE2 has **defective binding** to lipoprotein receptors, leading to impaired clearance of chylomicron and VLDL remnants. *Apo A* - Apo A-I is the main apolipoprotein of **HDL** and plays a crucial role in **reverse cholesterol transport**. - Deficiencies in Apo A-I are typically associated with conditions like **Tangier disease** or familial HDL deficiency, not type III hyperlipoproteinemia. *Apo B* - Apo B-100 is a key structural protein for **LDL** and VLDL, while Apo B-48 is essential for **chylomicrons**. - Defects in Apo B are associated with conditions like **familial hypercholesterolemia** (Apo B-100) or abetalipoproteinemia (Apo B-48), not primarily type III hyperlipoproteinemia. *Apo C* - Apo C-II is an activator of **lipoprotein lipase**, important for triglyceride hydrolysis. - Deficiencies in Apo C-II lead to **severe hypertriglyceridemia** (type I hyperlipoproteinemia), not directly broad beta disease.
Question 766: All are true about beta-oxidation except:
- A. Activation of FA is a must
- B. Carnitine palmitoyl transferase I is present in mitochondrial matrix. (Correct Answer)
- C. Carnitine palmitoyl transferase I is present in outer mitochondrial membrane
- D. Carnitine palmitoyl transferase II is present in inner mitochondrial membrane
Explanation: ***Carnitine palmitoyl transferase I is present in mitochondrial matrix.*** - **Carnitine palmitoyltransferase I (CPT I)** is located on the **outer mitochondrial membrane**, not the mitochondrial matrix. - Its role is to transfer the fatty acyl group from acyl-CoA to carnitine, forming **acylcarnitine** for transport into the mitochondria. - This is the **rate-limiting step** in fatty acid transport for beta-oxidation. *Activation of FA is a must* - **Fatty acids (FA)** must first be activated to **fatty acyl-CoA** in the cytosol before they can undergo beta-oxidation. - This activation step requires **ATP** and coenzyme A, catalyzed by **acyl-CoA synthetase**. *Carnitine palmitoyl transferase I is present in outer mitochondrial membrane* - **CPT I** is indeed located on the **outer mitochondrial membrane**, where it facilitates the conversion of fatty acyl-CoA to acylcarnitine. - This allows long-chain fatty acids to cross the mitochondrial membranes. *Carnitine palmitoyl transferase II is present in inner mitochondrial membrane* - **Carnitine palmitoyltransferase II (CPT II)** is located on the **inner mitochondrial membrane** (facing the matrix side). - It converts acylcarnitine back to **fatty acyl-CoA** inside the mitochondria, allowing beta-oxidation to proceed in the matrix.
Question 767: What is the major apolipoprotein of chylomicrons?
- A. B-48 (Correct Answer)
- B. B-100
- C. Apo-C
- D. Apo-E
Explanation: ***B-48*** - **Apolipoprotein B-48** is exclusively produced in the intestine and is the **major structural apolipoprotein** found only on **chylomicrons**. - It is critical for the **assembly and secretion of chylomicrons** from intestinal cells into the lymphatic system. - ApoB-48 represents the N-terminal 48% of ApoB-100 and lacks the LDL receptor-binding domain. *B-100* - **Apolipoprotein B-100** is synthesized in the liver and is the primary structural apolipoprotein of **VLDL, IDL, and LDL**. - It acts as the **ligand for the LDL receptor**, facilitating the uptake of cholesterol into cells. *Apo-C* - **Apolipoprotein C (Apo-C)** proteins (e.g., ApoC-II, ApoC-III) are exchangeable apolipoproteins found on several lipoproteins, including chylomicrons, VLDL, and HDL. - **ApoC-II activates lipoprotein lipase**, which hydrolyzes triglycerides, but these are **not structural proteins** and are present in smaller quantities. *Apo-E* - **Apolipoprotein E (Apo-E)** is acquired by chylomicrons in circulation and is important for **chylomicron remnant clearance** by the liver. - While present on chylomicrons, it is **not the major structural apolipoprotein** – that role belongs to ApoB-48.
Question 768: Which of the following is the MOST accurate statement regarding thromboxane A2?
- A. Formed by platelets
- B. Formed from PGG2/PGH2
- C. Prothrombogenic (Correct Answer)
- D. Vasoconstrictor
Explanation: ***ABCD*** - Thromboxane A2 is primarily **formed by platelets** [1] and is derived from **PGG2/PGH2**, having a significant role in **hemostasis**. - It is known to be **prothrombogenic** [1] and acts as a **vasoconstrictor** [2], enhancing platelet aggregation and promoting localized increases in **vascular resistance**. *ACB* - This option indicates only a partial representation of thromboxane A2's functions and formation. - It misses the comprehensive list of effects and does not mention it as a **vasoconstrictor** or its role in hemostasis. *ABC* - Like , it lacks recognition of all relevant characteristics of thromboxane A2. - Thus, it omits the **vasodilator** function, even though thromboxane A2 acts mainly as a **vasoconstrictor**. *ABCDE* - Including **E as vasodilator** contradicts the well-known actions of thromboxane A2, which does not promote vasodilation [2]. - Thus, this ssentially misrepresents thromboxane A2 as it primarily promotes **vasoconstriction** and is **prothrombogenic**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 130. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
Question 769: Which of the following is most strongly associated with heart disease?
- A. HDL
- B. LDL (Correct Answer)
- C. VLDL
- D. Chylomicrons
Explanation: ***LDL*** - **Low-density lipoprotein (LDL)** is often referred to as "bad cholesterol" because high levels contribute to the buildup of **plaque** in the arteries, leading to **atherosclerosis** and increasing the risk of heart disease. - **Elevated LDL** promotes cholesterol deposition in arterial walls, narrowing the vessels and impeding blood flow. *HDL* - **High-density lipoprotein (HDL)** is known as "good cholesterol" as it helps remove cholesterol from the arteries and transport it back to the liver for excretion. - **High HDL levels** are generally protective against heart disease, not associated with its development. *VLDL* - **Very-low-density lipoprotein (VLDL)** primarily transports **triglycerides** synthesized in the liver to various tissues. - While high VLDL levels can increase the risk of heart disease, primarily due to their breakdown into LDL, **LDL itself is a more direct and stronger predictor** of atherosclerotic disease. *Chylomicrons* - **Chylomicrons** are responsible for transporting **dietary fats** (triglycerides and cholesterol) from the intestines to the rest of the body after a meal. - Although high levels of chylomicrons can be associated with increased triglyceride levels, they are typically present for only a few hours after eating and are **not as strongly implicated in chronic atherosclerosis** as LDL.
Practice by Chapter
Lipid Classification and Chemistry
Practice Questions
Fatty Acid Oxidation
Practice Questions
Ketone Body Metabolism
Practice Questions
Fatty Acid Synthesis
Practice Questions
Metabolism of Triacylglycerols
Practice Questions
Phospholipid Metabolism
Practice Questions
Cholesterol Metabolism and Biosynthesis
Practice Questions
Bile Acids and Bile Salts
Practice Questions
Lipoprotein Metabolism and Transport
Practice Questions
Dyslipidemias and Atherosclerosis
Practice Questions
Prostaglandins and Eicosanoids
Practice Questions
Fatty Liver and Lipotropic Factors
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free