Multiple Choice Question on Lipid Metabolism (Cholesterol, Triglycerides, and Other Lipids)
1) The cholesterol serves as the precursor for the following biosynthetic pathways, EXCEPT
a) Bile acid synthesis
b) Steroid hormone synthesis
c) Aldosterone synthesis
d) Thyroid hormone synthesis
2) Which of the following lipids act as lungs surfactants?
a) Phosphatidylcholine
b) Phosphatidylethanolamine
c) Ceramide
d) Phosphatidylinositol
3) Identify the simple lipid from the following?
a) Lecithin
b) Fatty acid
c) Triacylglycerol
d) Steroids
4) All of the following are complex lipids, Except?
a) Phosphatidic acid
b) Cerebroside
c) Cardiolipin
d) Cholesterol
5) Which of the following is an essential fatty acid?
a) Linolenic acid
b) Arachidonic acid
c) Oleic acid
d) Palmitic acid
6) Bile acid is derived from:
a) Cholesterol
b) Amino acids
c) Fatty acids
d) Bilirubin
7) Which of the following lipid is mostly present in mitochondrial membranes?
a) Lecithin
b) Cephalin
c) Cardiolipin
d) Ceramide
8) Insulin enhances the uptake of triacylglycerols in adipose tissues.
a) Bile acid synthesis
b) Steroid hormone synthesis
c) Aldosterone synthesis
d) Thyroid hormone synthesis
2) Which of the following lipids act as lungs surfactants?
a) Phosphatidylcholine
b) Phosphatidylethanolamine
c) Ceramide
d) Phosphatidylinositol
3) Identify the simple lipid from the following?
a) Lecithin
b) Fatty acid
c) Triacylglycerol
d) Steroids
4) All of the following are complex lipids, Except?
a) Phosphatidic acid
b) Cerebroside
c) Cardiolipin
d) Cholesterol
5) Which of the following is an essential fatty acid?
a) Linolenic acid
b) Arachidonic acid
c) Oleic acid
d) Palmitic acid
6) Bile acid is derived from:
a) Cholesterol
b) Amino acids
c) Fatty acids
d) Bilirubin
7) Which of the following lipid is mostly present in mitochondrial membranes?
a) Lecithin
b) Cephalin
c) Cardiolipin
d) Ceramide
8) Insulin enhances the uptake of triacylglycerols in adipose tissues.
Which of the following enzyme is activated that facilitates the uptake?
a) Hormone-sensitive lipase
b) Lipoprotein lipase
c) LCAT
d) Apo C-II
9) Familial hypercholesterolemia is a genetic disorder of cholesterol metabolism.
a) Hormone-sensitive lipase
b) Lipoprotein lipase
c) LCAT
d) Apo C-II
9) Familial hypercholesterolemia is a genetic disorder of cholesterol metabolism.
The defect lies in the..............................................................................................
a) Transport of cholesterol from extrahepatic tissue to the liver
b) Impairment of cholesterol degradative pathway
c) Impairment of uptake of cholesterol by tissues
d) Impairment of HDL metabolism due to deficiency of Apo-A
10) Which of the following inhibits acetyl CoA carboxylase- a rate-limiting enzyme of fatty metabolism?
a) Citrate
b) ATP
c) Malonyl CoA
d) Acyl CoA
a) Transport of cholesterol from extrahepatic tissue to the liver
b) Impairment of cholesterol degradative pathway
c) Impairment of uptake of cholesterol by tissues
d) Impairment of HDL metabolism due to deficiency of Apo-A
10) Which of the following inhibits acetyl CoA carboxylase- a rate-limiting enzyme of fatty metabolism?
a) Citrate
b) ATP
c) Malonyl CoA
d) Acyl CoA
11) Acetyl CoA serves as the precursor for the synthesis of cholesterol, and the biosynthesis of cholesterol is tightly regulated.
Which of the following step is a regulatory step of cholesterol biosynthesis?
a) Formation 3-hydroxy-3-methylglutaryl COA
b) Formation of Mevalonate
c) Formation of Isoprenoid Unit
d) Formation of Lansterol
12) The enzyme that regulates the biosynthesis of cholesterol also serves as the druggable target for the reduction of hypercholesterolemia (increase blood cholesterol).
Identify the regulatory enzyme from the following options:
a) HMG-CoA synthase
b) HMG- CoA reductase
c) Lansterol oxidase
d) Cholesterol synthase
13) Which of the following hormone increases the synthesis of cholesterol by regulating the enzyme HMG CoA reductase?
a) Insulin
b) Glucagon
c) Glucocorticoids
d) All of the above
14) Sterol Regulatory Binding Protein binds to DNA at the sterol regulatory element to increase the expression of HMG CoA reductase, and synthesis of cholesterol.
What happens when there is the presence of a high cellular concentration of cholesterol?
a) Increases the proteolytic cleavage, release, and shuttling of SREBP into the nucleus
b) Decreases the proteolytic cleavage and release of SREBP from ER
c) Activates SREBP by inducing the conformational change
d) Inhibit SREBP by competitively binding to DNA binding site of SREBP
15) Hormones such as insulin & glucagon regulate HMG CoA reductase by a phosphorylation and dephosphorylation process.
Phosphorylation of HMG CoA reductase results in decreased enzyme activity.
Identify the correct statement from the following:
a) Insulin inhibits kinase that phosphorylates HMG CoA reductase
c) Insulin activates kinase that phosphorylates HMG CoA reductase
c) Insulin activates the phosphatase that removes a phosphate group from HMG CoA reductase
d) Insulin inhibits kinase that phosphorylates HMG CoA reductase
16) Hypercholesterolemia refers to a condition with high cholesterol with a serum cholesterol level of.............................................
a) >160 mg/dL
b) >200 mg/dL
c) >240 mg/dL
d) >280 mg/dL
17) Which of the following enzyme is responsible for the conversion of cholesterol to cholesterol ester inside the cells?
a) Lecithin Cholesterol Acyl Transferase
b) Acyl CoA Cholesterol Acyl Transferase
c) Cholesterol Esterase
d) None of the Above
18) Which of the following glycolytic intermediates serves as the precursor for the backbone for the synthesis of Triglycerides, Phosphatidylcholine, Phosphatidylethanolamine?
a) Glyceraldehyde-3-phosphate
b) Pyruvate
c) 1-3 Bisphosphoglycerate
d) 3-Phosphoglycerate
19) Ceramide is synthesized in the endoplasmic reticulum from the amino acid serine.
Ceramide is an important signaling molecule (second messenger) that regulates the pathways including which of the following process?
a) Apoptosis
b) cell senescence
c) cell differentiation
d) All of the above
20) Identify the phospholipid that possesses a surfactant activity and is synthesized shortly before parturition in full-term infants, and its deficiency in the lungs can cause respiratory distress syndrome.
a) Dipalmitoyl phosphatidyletholamine
b) Ceramide
c) Dipalmitoyl phosphatidylcholine
d) All of the above
What is the possible cause of the disease?
a) Tay Sachs Disease caused by Hexosaminidase A deficiency
b) Fabry Disease caused by Alpha-Galactosidase deficiency
c) Krabbe Disease caused by Beta-Galactosidase deficiency
d) Gaucher Disease caused by Beta-Glucosidase deficiency
Multiple Choice Answer Review:
1-d) Thyroid hormone synthesis
Cholesterol serves as a precursor for the biosynthesis of several important molecules in the body, including bile acids, steroid hormones, and aldosterone. However, it is not a precursor for the biosynthesis of thyroid hormones. The biosynthesis of thyroid hormones involves the incorporation of iodine into the amino acid tyrosine, which then undergoes several modifications to form the active thyroid hormones T3 and T4.
2-a) Phosphatidylcholine
Phosphatidylcholine (PC) is a major component of lung surfactant, which is a complex mixture of lipids and proteins that lines the inner surface of the lungs. Lung surfactant plays an important role in reducing the surface tension at the air-liquid interface within the alveoli of the lungs, thereby preventing their collapse during expiration and maintaining efficient gas exchange.
PC is the most abundant phospholipid in lung surfactant, accounting for approximately 70-80% of its total phospholipid content. It has a unique molecular structure, with a hydrophobic tail composed of two fatty acids and a hydrophilic head composed of choline and a phosphate group.
PC is the most abundant phospholipid in lung surfactant, accounting for approximately 70-80% of its total phospholipid content. It has a unique molecular structure, with a hydrophobic tail composed of two fatty acids and a hydrophilic head composed of choline and a phosphate group.
3-c) Triacylglycerol
Lipids can be classified into several categories based on their chemical structure and complexity. Two of the main categories of lipids are simple lipids and complex lipids.
Simple lipids: Simple lipids, also known as neutral lipids, are esters of fatty acids and various alcohols. They include triglycerides (which are composed of three fatty acids esterified to a glycerol molecule) and waxes (which are composed of long-chain fatty acids esterified to long-chain alcohols).
Complex lipids: Complex lipids, also known as compound lipids, are esters of fatty acids with a variety of other molecules, such as carbohydrates, amino acids, or phosphates. They include phospholipids (which are composed of a glycerol molecule esterified to two fatty acids and a phosphate group), sphingolipids (which are composed of a sphingosine backbone and a fatty acid chain), and glycolipids (which are composed of a carbohydrate molecule and a fatty acid chain).
Simple lipids: Simple lipids, also known as neutral lipids, are esters of fatty acids and various alcohols. They include triglycerides (which are composed of three fatty acids esterified to a glycerol molecule) and waxes (which are composed of long-chain fatty acids esterified to long-chain alcohols).
Complex lipids: Complex lipids, also known as compound lipids, are esters of fatty acids with a variety of other molecules, such as carbohydrates, amino acids, or phosphates. They include phospholipids (which are composed of a glycerol molecule esterified to two fatty acids and a phosphate group), sphingolipids (which are composed of a sphingosine backbone and a fatty acid chain), and glycolipids (which are composed of a carbohydrate molecule and a fatty acid chain).
4-d) Cholesterol
Complex lipids can be further subdivided into subclasses based on their additional molecular components, such as glycosphingolipids (which are composed of a carbohydrate chain and a sphingosine backbone) and phosphoglycerides (which are composed of a glycerol molecule esterified to two fatty acids, a phosphate group, and an additional polar molecule such as choline or serine)
5-a) Linolenic acid
An essential fatty acid is a type of fatty acid that cannot be synthesized by the human body and must be obtained through the diet. Of the options given, linolenic acid is the only essential fatty acid, while arachidonic acid, oleic acid, and palmitic acid are non-essential.
Linolenic acid is an omega-3 fatty acid that is important for the production of other omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These fatty acids are involved in many physiological processes, including the regulation of inflammation, blood clotting, and brain function. Linolenic acid is found in high amounts in foods such as flaxseeds, chia seeds, walnuts, and fatty fish.
Arachidonic acid is a non-essential omega-6 fatty acid that can be synthesized by the body from linoleic acid. It is involved in the production of signaling molecules called eicosanoids, which play a role in inflammation and immune function. Arachidonic acid is found in high amounts in animal products such as meat, eggs, and dairy.
Oleic acid and palmitic acid are both non-essential fatty acids that can be synthesized by the body. Oleic acid is an omega-9 fatty acid that is found in high amounts in olive oil and other plant-based oils. Palmitic acid is a saturated fatty acid that is found in high amounts in animal products such as meat and dairy, as well as in palm oil and coconut oil.
Linolenic acid is an omega-3 fatty acid that is important for the production of other omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These fatty acids are involved in many physiological processes, including the regulation of inflammation, blood clotting, and brain function. Linolenic acid is found in high amounts in foods such as flaxseeds, chia seeds, walnuts, and fatty fish.
Arachidonic acid is a non-essential omega-6 fatty acid that can be synthesized by the body from linoleic acid. It is involved in the production of signaling molecules called eicosanoids, which play a role in inflammation and immune function. Arachidonic acid is found in high amounts in animal products such as meat, eggs, and dairy.
Oleic acid and palmitic acid are both non-essential fatty acids that can be synthesized by the body. Oleic acid is an omega-9 fatty acid that is found in high amounts in olive oil and other plant-based oils. Palmitic acid is a saturated fatty acid that is found in high amounts in animal products such as meat and dairy, as well as in palm oil and coconut oil.
6-a) Cholesterol
Bile acids are a type of steroid molecule that are synthesized in the liver from cholesterol. Therefore, the correct answer to this question is (a) cholesterol.
Cholesterol is an essential precursor molecule for the biosynthesis of bile acids. In the liver, cholesterol is enzymatically converted to primary bile acids, such as cholic acid and chenodeoxycholic acid, through a series of enzymatic reactions involving several key enzymes, including cholesterol 7α-hydroxylase.
Once synthesized, primary bile acids are conjugated with taurine or glycine to form bile salts, which are secreted into the small intestine and play an important role in lipid digestion and absorption. In the small intestine, bile salts emulsify dietary fats, allowing pancreatic lipase to break them down into smaller fatty acids and monoglycerides that can be absorbed into the bloodstream.
After being secreted into the small intestine, bile acids are reabsorbed into the bloodstream and transported back to the liver for reuse in a process known as enterohepatic circulation. This recycling process is important for maintaining a constant supply of bile acids and conserving cholesterol.
Cholesterol is an essential precursor molecule for the biosynthesis of bile acids. In the liver, cholesterol is enzymatically converted to primary bile acids, such as cholic acid and chenodeoxycholic acid, through a series of enzymatic reactions involving several key enzymes, including cholesterol 7α-hydroxylase.
Once synthesized, primary bile acids are conjugated with taurine or glycine to form bile salts, which are secreted into the small intestine and play an important role in lipid digestion and absorption. In the small intestine, bile salts emulsify dietary fats, allowing pancreatic lipase to break them down into smaller fatty acids and monoglycerides that can be absorbed into the bloodstream.
After being secreted into the small intestine, bile acids are reabsorbed into the bloodstream and transported back to the liver for reuse in a process known as enterohepatic circulation. This recycling process is important for maintaining a constant supply of bile acids and conserving cholesterol.
7-c) Cardiolipin
Cardiolipin is a phospholipid that is predominantly found in the inner mitochondrial membrane, where it plays a critical role in mitochondrial function, including energy production and apoptosis. Lecithin and cephalin are also phospholipids, but they are more commonly found in cellular membranes, such as those in the liver and brain. Ceramide is a sphingolipid that is involved in signaling pathways and is found in the plasma membrane of cells.
8- b) Lipoprotein lipase
Insulin activates lipoprotein lipase (LPL) by increasing the expression of the LPL gene and promoting the translocation of LPL to the surface of adipocytes. LPL hydrolyzes triacylglycerol in circulating lipoproteins, such as chylomicrons and VLDL, releasing free fatty acids that are taken up by adipose tissue and stored as triacylglycerols. Hormone-sensitive lipase (HSL) is responsible for the breakdown of stored triacylglycerols in adipose tissue in response to hormonal signals, such as glucagon and epinephrine. LCAT and Apo C-II are involved in the metabolism of lipoproteins in the bloodstream.
9-c) Impairment of uptake of cholesterol by tissue
Familial hypercholesterolemia is a genetic disorder that results in high levels of cholesterol in the blood. The underlying defect in familial hypercholesterolemia is an impaired uptake of LDL (low-density lipoprotein) cholesterol by tissues, specifically the liver, due to a deficiency or dysfunction of LDL receptors. These receptors are responsible for removing LDL cholesterol from the bloodstream and transporting it into cells for use or degradation. In the absence of functional LDL receptors, LDL cholesterol accumulates in the blood and can lead to the development of atherosclerosis and cardiovascular disease. The other options listed in the question, such as impairment of cholesterol degradative pathway or HDL metabolism, are not characteristic features of familial hypercholesterolemia.
10-d) Acyl CoA
Malonyl CoA is also an inhibitor of acetyl CoA carboxylase. The presence of malonyl CoA signals that there is sufficient supply of fatty acids and inhibits the further synthesis of fatty acids by acetyl CoA carboxylase. This helps to prevent excessive accumulation of fatty acids and maintain a balance between synthesis and degradation of fatty acids.
Citrate and ATP are activators of acetyl CoA carboxylase, while acyl CoA is a substrate for fatty acid synthesis and does not inhibit acetyl CoA carboxylase.
11- b) Formation of Mevalonate
The biosynthesis of cholesterol is a complex process that occurs mainly in the liver and involves multiple enzymatic steps. The regulation of cholesterol synthesis occurs at various steps of this pathway, ensuring that the production of cholesterol meets the body's demand while avoiding the overproduction of cholesterol, which can lead to health problems.The key regulatory step in cholesterol biosynthesis occurs with the formation of mevalonate from 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) by the enzyme HMG-CoA reductase. This is a highly regulated step and is the target of cholesterol-lowering drugs called statins, which inhibit the activity of HMG-CoA reductase and thereby reduce cholesterol synthesis. Once mevalonate is formed, it is further metabolized to form isoprenoid units, which are key building blocks for the synthesis of cholesterol and other important biomolecules. Ultimately, cholesterol biosynthesis leads to the formation of lanosterol, which is further modified to produce cholesterol.
12-b) HMG- CoA reductase
HMG CoA reductase is an enzyme that catalyzes the conversion of HMG CoA to mevalonate, a key step in cholesterol biosynthesis. This enzyme is regulated by phosphorylation and dephosphorylation events, which are controlled by hormones such as insulin and glucagon.When HMG CoA reductase is phosphorylated, its activity is decreased, resulting in a decrease in cholesterol biosynthesis. Insulin, which is secreted in response to high blood glucose levels, activates a phosphatase enzyme that removes the phosphate group from HMG CoA reductase, thereby increasing its activity and promoting cholesterol biosynthesis.
On the other hand, glucagon, which is secreted in response to low blood glucose levels, activates a kinase enzyme that phosphorylates HMG CoA reductase, leading to its inhibition and a decrease in cholesterol biosynthesis.
13-a) Insulin
Insulin is a hormone secreted by the pancreas that plays a key role in regulating glucose and lipid metabolism. It increases the synthesis of cholesterol by stimulating the activity of the enzyme HMG CoA reductase, which is a rate-limiting enzyme in the biosynthesis of cholesterol. Glucagon, on the other hand, has the opposite effect and decreases the activity of HMG CoA reductase. Glucocorticoids can also increase the synthesis of cholesterol by upregulating the expression of HMG CoA reductase, among other mechanisms. However, insulin is the hormone most directly involved in the regulation of HMG CoA reductase activity.14-b) Decreases the proteolytic cleavage and release of SREBP from ER
When there is a high cellular concentration of cholesterol, it inhibits the activation of SREBP (Sterol Regulatory Binding Protein). In the presence of cholesterol, SREBP is retained in the endoplasmic reticulum (ER), and its proteolytic cleavage and release into the nucleus are reduced. SREBP activation requires its proteolytic cleavage and release from the ER, which is controlled by cholesterol levels. When cholesterol levels are high, the processing of SREBP is inhibited, preventing it from binding to the sterol regulatory element and promoting the transcription of genes involved in cholesterol synthesis, such as HMG CoA reductase.15-c) Insulin activates the phosphatase that removes a phosphate group from HMG CoA reductase
Insulin activates the phosphatase that removes a phosphate group from HMG CoA reductase. Insulin stimulates the dephosphorylation of HMG CoA reductase by activating a specific phosphatase enzyme. Dephosphorylation of HMG CoA reductase results in the activation of the enzyme and increased cholesterol synthesis. On the other hand, phosphorylation of HMG CoA reductase results in the inactivation of the enzyme and decreased cholesterol synthesis. Glucagon, which is released during fasting, activates a kinase that phosphorylates HMG CoA reductase, leading to its inactivation and decreased cholesterol synthesis.16-c) >240 mg/dL
Hypercholesterolemia refers to high levels of cholesterol in the blood, specifically a serum cholesterol level greater than 200 mg/dL. It is a major risk factor for the development of cardiovascular disease. The other options (a, c, and d) represent different cutoff values for serum cholesterol levels, but they do not accurately define hypercholesterolemia.17-b) Acyl CoA Cholesterol Acyl Transferase
Acyl CoA Cholesterol Acyl Transferase, also known as ACAT. ACAT catalyzes the esterification of cholesterol to cholesterol ester, which is an important mechanism for the storage of cholesterol within cells. Cholesterol esters are less hydrophilic than cholesterol and can be stored in lipid droplets, thus reducing the toxicity associated with excess free cholesterol. Lecithin Cholesterol Acyl Transferase (LCAT) is an enzyme that catalyzes the formation of cholesterol esters in the blood plasma, while Cholesterol Esterase is responsible for the reverse reaction, the hydrolysis of cholesterol esters back to free cholesterol.
Acyl CoA Cholesterol Acyl Transferase, also known as ACAT. ACAT catalyzes the esterification of cholesterol to cholesterol ester, which is an important mechanism for the storage of cholesterol within cells. Cholesterol esters are less hydrophilic than cholesterol and can be stored in lipid droplets, thus reducing the toxicity associated with excess free cholesterol. Lecithin Cholesterol Acyl Transferase (LCAT) is an enzyme that catalyzes the formation of cholesterol esters in the blood plasma, while Cholesterol Esterase is responsible for the reverse reaction, the hydrolysis of cholesterol esters back to free cholesterol.
18-a) Glyceraldehyde-3-phosphate
The glycolytic intermediate that serves as the precursor for the backbone for the synthesis of triglycerides, phosphatidylcholine, and phosphatidylethanolamine is glycerol-3-phosphate. Glycerol-3-phosphate is produced from dihydroxyacetone phosphate and glyceraldehyde-3-phosphate through the action of glycerol-3-phosphate dehydrogenase. Glycerol-3-phosphate can be esterified with fatty acids to form triglycerides or can be converted to phosphatidylcholine and phosphatidylethanolamine through a series of reactions involving cytidine triphosphate (CTP) and the addition of various functional groups. 19-d) All of the above
Ceramide is an important signaling molecule that plays a role in regulating several cellular processes, including apoptosis, cell senescence, and cell differentiation.Apoptosis, also known as programmed cell death, is a highly regulated process that eliminates damaged or unwanted cells. Ceramide has been shown to play a key role in regulating apoptosis by activating signaling pathways that lead to cell death.
Cell senescence refers to the irreversible arrest of cell growth and division. Ceramide has been implicated in the regulation of cellular senescence by activating pathways that promote senescence.
Cell differentiation refers to the process by which cells develop specialized functions and structures. Ceramide has been shown to play a role in regulating cell differentiation by activating signaling pathways that promote differentiation.
20-c) Dipalmitoyl phosphatidylcholine
The phospholipid that possesses a surfactant activity and is synthesized shortly before parturition in full-term infants is dipalmitoyl phosphatidylcholine (DPPC). Surfactant is a mixture of phospholipids and proteins that is produced by the type II alveolar cells of the lungs. DPPC is the major phospholipid component of surfactant, and its primary function is to reduce the surface tension at the air-liquid interface in the lungs. This helps to prevent the collapse of the alveoli during exhalation and promotes normal breathing.Deficiency of DPPC in the lungs can cause respiratory distress syndrome (RDS), which is a common problem in premature infants. In premature infants, the production of surfactant may not be fully developed, resulting in inadequate surfactant levels in the lungs. This can lead to breathing difficulties, which can be life-threatening if not treated promptly.
21-a) Tay Sachs Disease caused by Hexosaminidase A deficiency
The clinical presentation of mental retardation, blindness, and muscular weakness, along with the biochemical finding of GM2 ganglioside accumulation in tissues, is indicative of a lysosomal storage disorder called Tay-Sachs disease.Tay-Sachs disease is a rare genetic disorder caused by a deficiency in the enzyme hexosaminidase A, which leads to the accumulation of GM2 gangliosides in the brain and nerve cells. This accumulation causes progressive damage to these cells, leading to the symptoms observed in affected individuals.
The disease is inherited in an autosomal recessive manner, meaning that an affected individual must inherit two copies of the defective gene (one from each parent) to develop the disease