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biochem 2 > membrane lipid synthesis 2 > Flashcards

membrane lipid synthesis 2 Flashcards

1
Q

What are the primary sites of cholesterol biosynthesis in the body?
a) Kidneys and lungs
b) Brain and heart
c) Liver and intestine
d) Muscle and adipose tissue

A

c) Liver and intestine

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2
Q

Which enzyme catalyzes the synthesis of mevalonate, a precursor in cholesterol biosynthesis?
a) HMG CoA reductase
b) ATP synthase
c) Phospholipase A2
d) Lipoprotein lipase

A

a) HMG CoA reductase

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3
Q

What mediates changes in the rate of cholesterol formation primarily?
a) Availability of dietary cholesterol
b) Activity of SREBP
c) Changes in cell membrane fluidity
d) Amount and activity of HMG CoA

A

d) Amount and activity of HMG CoA

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4
Q

Which transcription factor regulates the proteins required for lipid synthesis, including cholesterol?
a) SREBP
b) NF-κB
c) AP-1
d) STAT

A

a) SREBP

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5
Q

Where does sterol regulatory element binding protein (SREBP) reside in the cell?
a) Golgi complex
b) Endoplasmic reticulum (ER)
c) Nucleus
d) Mitochondria

A

b) Endoplasmic reticulum (ER)

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6
Q

What is SREBP bound to in the ER?
a) DNA-binding domain
b) Serine protease
c) Sterol regulatory element
d) SREBP cleavage activating protein (SCAP)

A

d) SREBP cleavage activating protein (SCAP)

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7
Q

What triggers the movement of SCAP and SREBP to the Golgi complex?
a) High cholesterol levels
b) Low cholesterol levels
c) Increased gene expression
d) Presence of lipid droplets

A

b) Low cholesterol levels

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8
Q

Which proteases are involved in the proteolytic cleavages of SREBP in the Golgi complex?
a) Metalloprotease and caspase
b) Serine protease and caspase
c) Serine protease and metalloprotease
d) Metalloprotease and endopeptidase

A

c) Serine protease and metalloprotease

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9
Q

What happens to the SREBP when cholesterol levels rise?
a) It is released from SCAP and translocates to the nucleus.
b) It is rapidly degraded by proteasomes located in the nucleus.
c) It undergoes proteolytic cleavage in the Golgi complex.
d) It binds to Insig and is transported to the Golgi complex.

A

b) It is rapidly degraded by proteasomes located in the nucleus.

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10
Q

How does cholesterol affect SCAP’s interaction with Insig?
a) Cholesterol enhances the binding of SCAP to Insig.
b) Cholesterol inhibits the binding of SCAP to Insig.
c) Cholesterol has no effect on the interaction between SCAP and Insig.
d) Cholesterol promotes the degradation of Insig.

A

a) Cholesterol enhances the binding of SCAP to Insig.

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11
Q

What role does Insig play in the regulation of cholesterol biosynthesis?
a) It promotes the release of SREBP from SCAP.
b) It inhibits the degradation of SREBP in the nucleus.
c) It facilitates the transcription of genes involved in cholesterol biosynthesis.
d) It prevents the transport of SREBP from the ER to the Golgi complex.

A

d) It prevents the transport of SREBP from the ER to the Golgi complex.

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12
Q

Which cellular structure is primarily responsible for the degradation of SREBP in the nucleus?
a) Endoplasmic reticulum (ER)
b) Golgi complex
c) Nucleus
d) Proteasomes

A

d) Proteasomes

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13
Q

How are structural changes in the membrane domain of the reductase induced?
a) By decreasing concentrations of sterols
b) By increasing concentrations of sterols
c) By binding to Insigs
d) By undergoing polyubiquitination

A

b) By increasing concentrations of sterols

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14
Q

What happens to the reductase when it binds to a subset of Insigs associated with ubiquitinating enzymes?
a) It is extracted from the membrane and degraded.
b) It undergoes polyubiquitination.
c) It induces structural changes in the membrane.
d) It activates sterol synthesis.

A

a) It is extracted from the membrane and degraded.

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15
Q

What is the consequence of increasing concentrations of sterols on the reductase?
a) It induces polyubiquitination.
b) It prevents the binding of Insigs.
c) It stabilizes the reductase.
d) It enhances the enzymatic activity of the reductase.

A

c) It stabilizes the reductase.

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16
Q

Which cellular process is responsible for the degradation of the reductase?
a) Endocytosis
b) Autophagy
c) Ubiquitination followed by proteasomal degradation
d) Glycosylation

A

c) Ubiquitination followed by proteasomal degradation

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17
Q

What is the primary function of lipoprotein particles?
a) To store cholesterol in body fluids
b) To transport cholesterol and triacylglycerols throughout the body
c) To synthesize cholesterol in tissues
d) To degrade cholesterol in the liver

A

b) To transport cholesterol and triacylglycerols throughout the body

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18
Q

How are the fatty acid constituents of the triacylglycerol components of lipoprotein particles utilized?
a) They are excreted by the liver.
b) They are incorporated into phospholipids for membrane synthesis.
c) They are converted into glucose for energy production.
d) They are stored in adipose tissue for later use.

A

b) They are incorporated into phospholipids for membrane synthesis.

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19
Q

Why is cholesterol considered a vital component of membranes?
a) It serves as an energy source for cells.
b) It acts as a precursor to steroid hormones.
c) It provides structural support to cell walls.
d) It facilitates nerve transmission in the brain.

A

c) It provides structural support to cell walls.

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20
Q

How does high-density lipoprotein (HDL) contribute to cholesterol metabolism?
a) It stores cholesterol in body tissues.
b) It transports cholesterol from the liver to body tissues.
c) It picks up cholesterol released into the plasma and delivers it to the liver for excretion.
d) It synthesizes cholesterol in the liver.

A

c) It picks up cholesterol released into the plasma and delivers it to the liver for excretion.

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21
Q

What is the main function of lipoprotein lipases in relation to chylomicrons?
a) They stabilize the structure of chylomicrons.
b) They transport cholesterol in chylomicrons.
c) They hydrolyze triacylglycerols in chylomicrons for release.
d) They facilitate the uptake of chylomicrons by the liver.

A

c) They hydrolyze triacylglycerols in chylomicrons for release.

22
Q

What stabilizes very low-density lipoproteins (VLDL) in the blood?
a) Apolipoprotein B-48
b) Apolipoprotein E
c) Apolipoprotein B-100
d) Lipoprotein lipases

A

c) Apolipoprotein B-100

23
Q

What are intermediate-density lipoproteins (IDL) rich in?
a) Triacylglycerols
b) Phospholipids
c) Cholesteryl esters
d) Free fatty acids

A

c) Cholesteryl esters

24
Q

What are the two fates of intermediate-density lipoproteins (IDL) after lipases hydrolyze triacylglycerols from them?
a) They are transported to adipose tissue for storage.
b) They are converted into high-density lipoproteins (HDL).
c) They are taken up by the liver for processing or converted into low-density lipoproteins (LDL).
d) They are released into the bloodstream for immediate energy use.

A

c) They are taken up by the liver for processing or converted into low-density lipoproteins (LDL).

25
Q

What is the main role of Low-Density Lipoproteins (LDL) in the bloodstream?
a) Transporting triglycerides to adipose tissue
b) Facilitating cholesterol synthesis in the liver
c) Acting as a major carrier of cholesterol
d) Regulating glucose levels in the blood

A

c) Acting as a major carrier of cholesterol

26
Q

What is the primary component of the core of LDL particles?
a) Triglycerides
b) Phospholipids
c) Free fatty acids
d) Cholesterol esters

A

d) Cholesterol esters

27
Q

What is the function of Apolipoprotein B-100 (apo B-100) in LDL particles?
a) Binding to target cells
b) Catalyzing cholesterol synthesis
c) Facilitating triglyceride breakdown
d) Enhancing phospholipid synthesis

A

a) Binding to target cells

28
Q

What process is involved in the uptake of LDL particles by cells?
a) Receptor-mediated exocytosis
b) Facilitated diffusion
c) Receptor-mediated endocytosis
d) Passive transport

A

c) Receptor-mediated endocytosis

29
Q

What initiates the process of receptor-mediated endocytosis of LDL particles?
a) Binding of ATP to the LDL receptor
b) Interaction between Apolipoprotein B-100 and a specific plasma membrane receptor
c) Activation of lysosomes in the cytoplasm
d) Fusion of LDL-containing vesicles with lysosomes

A

b) Interaction between Apolipoprotein B-100 and a specific plasma membrane receptor

30
Q

What happens to the plasma membrane during receptor-mediated endocytosis of LDL particles?
a) It releases LDL particles into the bloodstream
b) It undergoes fusion with lysosomes
c) It invaginates to form an endosome
d) It becomes permeable to LDL receptors

A

c) It invaginates to form an endosome

31
Q

What is responsible for acidifying the endosome during receptor-mediated endocytosis?
a) ATP-dependent proton pump
b) Clathrin-coated pits
c) Lysosomal enzymes
d) LDL receptors

A

a) ATP-dependent proton pump

32
Q

What genetic disease results from the absence or deficiency of functional LDL receptors?
a) Atherosclerosis
b) Familial hypercholesterolemia
c) Hyperlipidemia
d) Coronary artery disease

A

b) Familial hypercholesterolemia

33
Q

What happens to excess LDL in individuals with familial hypercholesterolemia?
a) It is excreted through the kidneys
b) It becomes oxidized and taken up by macrophages
c) It is metabolized into bile acids in the liver
d) It is converted into high-density lipoproteins (HDL)

A

b) It becomes oxidized and taken up by macrophages

34
Q

What role do foam cells play in atherosclerosis?
a) They contribute to the formation of blood clots
b) They release anti-inflammatory cytokines
c) They become trapped in blood vessels and form plaques
d) They stimulate the production of LDL receptors

A

c) They become trapped in blood vessels and contribute to the formation of atherosclerotic plaques.

35
Q

What role does PCSK9 protease play in regulating LDL receptor cycling?
a) It promotes the release of LDL from the endosome
b) It binds to the LDL receptor, facilitating LDL uptake
c) It converts the LDL receptor from an open to a closed structure
d) It binds to the LDL receptor, locking it in the open conformation

A

d) It binds to the LDL receptor, locking it in the open conformation

36
Q

What happens to the LDL receptor when PCSK9 binds to it?
a) The receptor is recycled back to the cell surface
b) The receptor is degraded in the lysosome along with its LDL cargo
c) The receptor undergoes conformational changes, enhancing LDL uptake
d) The receptor forms a stable complex with PCSK9, preventing LDL binding

A

b) The receptor is degraded in the lysosome along with its LDL cargo

37
Q

Which cellular compartment is responsible for the degradation of the LDL receptor along with its LDL cargo?
a) Golgi apparatus
b) Endoplasmic reticulum
c) Endosome
d) Lysosome

A

d) Lysosome

38
Q

How do reduced levels of PCSK9 affect LDL levels in the blood?
a) They increase LDL levels by promoting LDL receptor cycling
b) They decrease LDL levels by inhibiting LDL receptor cycling
c) They increase LDL levels by inhibiting LDL receptor degradation
d) They decrease LDL levels by enhancing LDL receptor degradation

A

b) They decrease LDL levels by inhibiting LDL receptor cycling

39
Q

Which process is associated with HDL in protecting against atherosclerosis?
a) LDL transport
b) Reverse cholesterol transport
c) Foam cell formation
d) Plaque formation

A

b) Reverse cholesterol transport

40
Q

What is the primary function of HDL in reverse cholesterol transport?
a) Removing cholesterol from the liver
b) Transporting cholesterol to peripheral tissues
c) Removing cholesterol from cells, especially macrophages
d) Facilitating the formation of plaques

A

c) Removing cholesterol from cells, especially macrophages

41
Q

Which steroid hormone is responsible for preparing the lining of the uterus for implantation and preventing premature uterine contractions?
a) Progesterone
b) Glucocorticoids
c) Aldosterone
d) Testosterone

A

a) Progesterone

42
Q

What is the primary function of glucocorticoids such as cortisol?
a) Enhancing fat and protein synthesis
b) Inhibiting the inflammatory response
c) Increasing blood volume and pressure
d) Promoting the development of male secondary sex characteristics

A

b) Inhibiting the inflammatory response

43
Q

Which steroid hormone acts primarily on the distal tubules of the kidney to regulate electrolyte balance?
a) Progesterone
b) Glucocorticoids
c) Mineralocorticoids
d) Androgens

A

c) Mineralocorticoids

44
Q

What is the initial step in the hydroxylation of steroids by cytochrome P450 monooxygenases?
a) Oxygen binds to Fe2+
b) Adrenodoxin donates an electron
c) Substrate binds to the enzyme
d) The Fe4+ = O intermediate abstracts a hydrogen atom from the substrate

A

c) Substrate binds to the enzyme

45
Q

Which molecule donates electrons to reduce the heme iron in cytochrome P450 during steroid hydroxylation?
a) Oxygen
b) Water
c) Adrenodoxin
d) Substrate radical

A

c) Adrenodoxin donates an electron

46
Q

What happens in step 5 of the hydroxylation process?
a) A molecule of water is released
b) The Fe4+ = O intermediate abstracts a hydrogen atom
c) The bond between the oxygen atoms is cleaved
d) Adrenodoxin donates a second electron

A

a) A molecule of water is released

47
Q

What is the first step in the synthesis of progesterone from pregnenolone?
a) Isomerization of a double bond
b) Oxidation of a hydroxyl group
c) Reduction of a carbonyl group
d) Esterification of a carboxyl group

A

b) Oxidation of a hydroxyl group

48
Q

Which functional group is formed in step 1 of the synthesis process?
a) Hydroxyl group
b) Ketone group
c) Carboxyl group
d) Ester group

A

b) Ketone group

49
Q

What is the final change in step 2 of the synthesis process?
a) Formation of a double bond
b) Formation of a hydroxyl group
c) Isomerization of a double bond
d) Reduction of a ketone group

A

a) Formation of a double bond

50
Q

What initiates the synthesis of vitamin D from 7-dehydrocholesterol?
a) Exposure to infrared light
b) Absorption of ultraviolet light
c) Oxidation by cytochrome P450 enzymes
d) Hydrolysis by lipases

A

b) Absorption of ultraviolet light

51
Q

Which condition is associated with a deficiency of vitamin D?
a) Scurvy
b) Rickets
c) Beriberi
d) Pellagra

A

b) Rickets

52
Q

What is the consequence of vitamin D deficiency in children?
a) Weakness of muscles
b) Inadequate calcification of bone
c) Night blindness
d) Increased risk of scurvy

A

b) Inadequate calcification of bone

biochem 2 (6 decks)

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