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Lipoproteins Flashcards

The types of lipidaemia are based on the Fredrickson classification. (102 cards)

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1
Q

State the function of lipoproteins.

A

Lipoproteins is the mechanism used for the efficient transportation of lipids around the body.

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2
Q

What is a steroid hormone?

A

A steroid hormone is a type of hormone derived from cholesterol.

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3
Q

Is cholesterol a component of cellular plasma membranes?

A

Yes

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4
Q

What is cholesterol a precursor to?

A

Bile acids and steroids

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5
Q

Is cholesterol essential in diets?

A

No

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6
Q

What is the precursor for cholesterol?

A

Polymerised isoprene units

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7
Q

Maximally, how much cholesterol can the human body synthesise per day?

A

800mg per day on a low cholesterol diet

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8
Q

What is the major step of cholesterol biosynthesis?

A

The rate-limiting, “major” step of cholesterol biosynthesis is:
Acetoacetyl CoA + Acetly CoA = 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). Catalysed by HMG CoA synthase and converts H2O to CoA.
This is then converted to mevalonate in the cytosol and the reaction is reversed in the mitochondria.

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9
Q

What are the steroid hormones?

A

Progestagens, mineralocorticoids, glucocorticoids, androgens, oestrogens.

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10
Q

Define progestagen.

A

The primary progestagen is progesterone, produced in the corpus luteum. It prepares the lining of the uterus for the implantation of the ovum and is essential for the maintenance of pregnancy.

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11
Q

Define glucocorticoid.

A

The primary glucocorticoid is cortisol, produced in the adrenal cortex. Cortisol promoted gluconeogenesis, glycogen synthesis, lipid and protein degeneration and inhibits inflammatory response. It is secreted as a response to stress.

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12
Q

Define mineralocorticoid.

A

The primary mineralocorticoid is aldosterone, produced in the adrenal cortex. It acts on the distal tubule of the kidney to increase absorption of Na+ and excretion of K+ and H+. It increases blood volume and blood pressure.

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13
Q

What type of cholesterol is considered dangerous?

A

Unesterfied cholesterol

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14
Q

What makes esterified cholesterol safe(r)?

A

Cholesterol is made more hydrophobic, it is easier to store in lipid molecules, making it less toxic.

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15
Q

What is endocytosis?

A

Endocytosis is the process by which cells engulf external substances, into their cytoplasm by enclosing them in a vesicle.

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16
Q

Describe the regulation of intracellular cholesterol.

A

Low-density lipoprotein (LDL) enters the cell by binding to the LDL receptor. After endocytosis, LDL undergoes lysosomal action to release free cholesterol. Free cholesterol is converted into cholesterol esters by acyl-CoA: cholesterol acyl transferase (ACAT). These cholesterol esters are stored in lipid droplets.

FEEDBACK MECHANISM
When intracellular cholesterol levels are low HMG-CoA reductase is activated to produce more cholesterol. LDL receptor expression (transcription of the gene) is increased to import cholesterol from LDL in the blood.
High levels of intracellular cholesterol inhibit HMG-CoA reductase (the enzyme that catalyses the rate-limiting reaction of cholesterol synthesis). This prevents further synthesis. ACAT is activated and LDL receptor expression is supressed.

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17
Q

How do insulin and glucagon regulate the activity of HMG-CoA reductase?

A

Insulin activates HMG CoA reductase by simulating phosphatase activity, which dephosphorylates and activates the enzyme. This promotes cholesterol synthesis. Glucagon inhibits HMG CoA reductase by stimulating kinase activity, which phosphorylates and inactivates the enzyme, reducing cholesterol synthesis.

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18
Q

At what levels is the activity of HMG CoA reductase regulated?

A

The gene transcription (mRNA synthesis) of HMG CoA reductase may be suppressed or promoted. The enzyme may be phosphorylated or dephosphorylated.

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19
Q

How do bile salts regulate the activity of HMG-CoA reductase?

A

Cholesterol is converted to bile salts in the liver. An increased level of bile salts indicates an adequate supply of cholesterol. Negative feedback is seen, the level of bile salts affects cholesterol synthesis in the liver, it is affected by suppression of the enzyme’s gene transcription. High bile salts reduce the uptake of cholesterol by LDL receptors. Bile salts indirectly activate AMP-activated protein kinase (AMPK), which phosphorylates HMG-CoA reductase, rendering it inactive.

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20
Q

Which type of cholesterol is considered bad and why?

A

LDL cholesterol is considered bad because its the lipoprotein that transports cholesterol to peripheral tissues. Accumulation of this cholesterol becomes oxidised and becomes pathogenic.
(B-100)

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21
Q

Which type of cholesterol is considered good and why?

A

HDL cholesterol is considered good because this is the lipoprotein which removes excess cholesterol from the periphery and returns it to the liver for metabolism. (A)

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22
Q

What is the source and function of very low density lipoproteins (VLDL)? State its apoproteins.

A

VLDL is produced in the liver. It is responsible for the transport of endogenously synthesised triacylglycerol. B-100, C, E

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23
Q

What is the source and function chylomicrons? State its apoproteins.

A

CM is produced in the intestine. It is responsible for the transport of dietary triacylglycerol. B-48, C, E

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24
Q

List the classes of lipoproteins by ascending size.

A

HDL, LDL, VLDL, CM

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25
State the action and site of action of lipoprotein lipase.
LPL hydrolyses triglycerides found in lipoproteins (CM, VLDL) into free fatty acids and glycerol. Acts on endothelial cell surfaces.
26
State the action and site of action of Acetyl CoA: cholesterolacyltransferase.
ACAT converts cholesterol to cholesterol esters intracellularly. Acts in the endoplasmic reticulum.
27
State the action and site of action of lecithin: cholesterolacytransferase.
LCAT converts cholesterol to cholesterol esters in blood via HDLs. Acts in the blood plasma.
28
State the action and site of action of cholesterol ester transfer protein.
CETP transfers cholesterol esters from HDL to VLDL in a exchange for triglycerides. Acts in the blood plasma.
29
State the action and site of action of ATP-binding cassette transporters
ABC transporters acts in the plasma membrane of cells to regulate cholesterol removal from cells to HDLs.
30
State the function of the A-I apolipoprotein.
A-I activates LCAT and plays a structural role in HDL.
31
State the function of the B-100 apolipoprotein.
B-100 plays a structural role in LDL, IDL and VLDL. It aids in receptor binding.
32
State the function of the B-48 apolipoprotein.
B-48 plays a structural role in chylomicrons.
33
State the function of the C-I apolipoprotein.
C-1 is a cofactor of LCAT.
34
State the function of the C-II apolipoprotein.
C-II is an activator of LPL.
35
State the function of the C-III apolipoprotein.
C-III inhibits LPL, it inhibits the clearance of the remnant particles of CM and VLDL.
36
State the function of the E apolipoprotein.
E aids in binding between LDL and remnant/scavenger receptors.
37
How does atherosclerosis develop?
Initially develops due to a weakening in the endothelium. LDL particles infiltrate the intima of the arterial wall. LDL is oxidised, becoming pro-inflammatory and chemotactic. Macrophages engulf oxidised LDL, forming foam cells which aggregate, leaving fatty streaks. A fibrous cap develops due to inflammation. Arterial blockages may lead to myocardial infarctions or strokes.
38
Describe the digestion of triacylglycerides in the intestinal lumen.
Bile salts from the gallbladder emulsify the TAGs, increasing surface area or enzyme action. Pancreatic lipase hydrolyzes TAGs at the sn-1 and 3 positions, releasing 2 free fatty acids and a 2-monoacylglycerol. These products are absorbed into the intestinal cells for re-esterification and packaging into chylomicrons. Colipase ensures lipase remains active in the presence of bile salts. Phospholipase A2 hydrolyzes dietary phospholipids. FFAs, 2-MAGs, fat-soluble vitamins and bile salts form mixed micelles. These micelles transport lipids across the aqueous lumen to epithelial cells.
39
The apoprotein B-48 is only found in one class of cholesterol, which is this?
Chylomicrons
40
What shape are HDLs?
Discoidal
41
Where are HDLs made?
In the intestine and liver
42
What function do HDLs have in maturing chylomicrons?
Chylomicrons mature as they receive the apoproteins C-II and E from HDL. HDLs behave in a similar way toward VLDLs.
43
What is the fate of chylomicron remnants?
Chylomicron remnants are taken up by the liver via receptors for ApoE.
44
Explain how the liver produces VLDLs.
The liver synthesises triglycerides from free fatty acids and glycerol. Cholesterol is produced in the liver or obtained from the bloodstream. In hepatocytes, triglycerides, cholesterol and apolipoproteins (ApoB-100) are assembled to form nascent VLDLs. This occurs in the Golgi apparatus and endoplasmic reticulum. These nascent VLDLs are secreted into the bloodstream by exocytosis.
45
What are enterocytes?
Intestinal cells
46
State the twofold function of insulin in lipid transport.
Insulin stimulates the transport of glucose into adipocytes via GLUT4 transporters, to provide glycerol-3-phosphate for TG synthesis. It also stimulates the synthesis and secretion of LPL.
47
Explain the conversion of fatty acids in the triglycerides of chylomicrons and VLDLs to the triglycerides stored in adipose cells.
As chylomicrons and VLDL circulate in the bloodstream, LPL hydrolyzes the TGs in these lipoproteins into free fatty acids (FFA) and glycerol. These FFAs are are released into the bloodstream and taken up by adipocytes. They are taken up by fatty acid transport proteins. Inside adipocytes, FFAs are primarily re-esterified to form triacylglycerols (TG) for storage. Once inside, fatty acids are activated by acyl CoA synthetase, forming fatty acyl-CoA. Fatty acyl-CoA molecules are esterified with glycerol-3-phosphate to form TGs. These TGs are stored in lipid droplets within the adipocytes, providing a long-term energy reserve.
48
What is the fate of VLDLs?
After VLDLs perform their duty, the resulting IDLs may be taken up by the liver (via ApoB-100 receptors) or progress to LDLs by losing more TGs. LDLs are taken up by peripheral tissues or the liver, using the same receptors.
49
State the function of cholesterol ester transfer protein (CETP).
CETP transfers cholesterol esters from HDLs to VLDLs in exchange for TGs.
50
What transporters are responsible for the efflux of cholesterol from peripheral tissues to HDLs
ABCA1 and ABCG1
51
What is a desirable level of total cholesterol?
Less than 200mg/dL, at a concentration of 5.1 mmol/L
52
Define lipidaemia.
Lipidaemia is the presence of abnormal levels of lipids in the blood.
53
What are the biochemical symptoms of type I lipidaemia?
LPL deficiency, resulting in elevated TGs and CMs
54
What are the biochemical symptoms of type IIa lipidaemia?
A mutation in the LDL receptor gene is seen. TGs are normal, but LDL is increased.
55
What are the biochemical symptoms of type IIb lipidaemia?
Increased TGs, VLDLs and a decreased clearance of LDL. Also genetic.
56
What are the biochemical symptoms of type III lipidaemia?
Increased TGs, IDLs and VLDLs. It is associated with early onset cardiovascular disease.
57
What are the biochemical symptoms of type IV lipidaemia?
Familial hypertriglyceridemia (increased TGs) and increased VLDLs.
58
What are the biochemical symptoms of type V lipidaemia?
High TGs and VLDLs
59
State the normal levels of TGs, LDLs, CMs, VLDLs, IDLs and HDLs.
Note: these tests are taken at least 9 hours following a meal, in a fasted state. TG: below 1.7mmol/L LDL: below 2.6mmol/L CM: undetectable VLDL: TG/2.22 IDL: total cholesterol - LDL - HDL HDL: below 1mmol/L
60
What is dyslipidaemia?
Abnormal levels of lipids in the bloodstream.
61
Explain enterohepatic circulation.
Enterohepatic circulation is the recycling of bile salts between the liver, intestine, and gallbladder, ensuring the digestion and conservation of bile components. The liver synthesizes bile salts from cholesterol (0.2–0.6 g/day). It also reconjugates secondary bile salts. The bile salts are stored in the gallbladder before being released into the intestine. Bile salts aid in the digestion and absorption of fats in the intestine. Around 12–32 g/day of bile salts are reabsorbed in the intestine and returned to the liver. The efficiency of reabsorption is greater than 95%. A pool of bile salts (2–4 g) is present and undergoes 6–8 cycles per day. Gut bacteria deconjugate and dehydroxylate bile salts, producing secondary bile salts. The reabsorbed bile salts enter the liver through the portal circulation for recycling. A small fraction (<5%, or 0.2–0.6 g/day) of bile salts is lost in feces.
62
What is the main driver for atherosclerotic plaque formation and development?
LDL cholesterol
63
What is a foam cell?
A foam cell is a swollen macrophage with lipid inclusions.
64
State the developmental stages of atherosclerosis.
Lesion initiation, fatty streak, fibrous plaque, plaque rupture
65
What biomarker is used as a marker of oxidative stress in vivo and is involved in the early stages of atherosclerosis?
F2-isoprostanes (F2-IsoPs)
66
Which lipid-related biomarker contributes to the initiation of atherosclerosis through oxidation and foam cell formation?
Oxidized LDL (OxLDL)
67
What inflammatory biomarkers are elevated in the early stages of atherosclerosis and indicate endothelial dysfunction?
Asymmetric dimethylarginine (ADMA), microalbumin, and high-sensitivity C-reactive protein (hsCRP)
68
Which enzymes are involved in plaque maturation and vulnerability, contributing to oxidative stress and inflammation?
Myeloperoxidase (MPO) and lipoprotein-associated phospholipase A2 (Lp-PLA2)
69
What cardiac biomarkers indicate acute coronary syndrome and myocardial damage?
Troponin T and creatine kinase-MB (CK-MB)
70
How does microalbuminuria serve as a cardiovascular risk marker?
It indicates endothelial dysfunction and is associated with increased cardiovascular morbidity and mortality, particularly in patients with hypertension or diabetes.
71
What is the role of hsCRP in atherosclerosis progression?
It is an acute-phase reactant produced by the liver in response to inflammation, and elevated levels correlate with increased cardiovascular risk.
72
What role does Lp-PLA2 play in atherosclerosis?
It is an enzyme involved in the breakdown of oxidized phospholipids, promoting inflammation and plaque instability.
73
Which biomarker is crucial for diagnosing myocardial infarction due to its high specificity for cardiac muscle injury?
Troponin T
74
What is the genetic defect in familial hypercholesterolemia?
Reduced numbers of functional LDL receptors
75
What is the Fredrickson classification of familial hypercholesterolemia?
Type IIa or IIb
76
What is the major risk associated with familial hypercholesterolemia?
Coronary heart disease
77
What causes familial hypertriglyceridemia?
Possibly a single gene defect
78
What is the Fredrickson classification of familial hypertriglyceridemia?
Type IV/V
79
What causes familial combined hyperlipidemia?
Possibly a single gene defect
80
What is the Fredrickson classification of familial combined hyperlipidemia?
Type IIa, IIb, IV, or V
81
What is the major risk associated with familial combined hyperlipidemia?
Coronary heart disease
82
What is the genetic defect in lipoprotein lipase deficiency?
Low levels of functional LPL
83
What is the Fredrickson classification of lipoprotein lipase deficiency?
I
84
What is the major risk associated with lipoprotein lipase deficiency?
Pancreatitis
85
What is the genetic defect in Apo C-II deficiency?
Inability to synthesize apo C-II (a cofactor for lipoprotein lipase)
86
What is the Fredrickson classification of Apo C-II deficiency?
I
87
What is the major risk associated with Apo C-II deficiency?
Pancreatitis
88
What is the genetic defect in abetalipoproteinemia?
Inability to synthesize apo B
89
What is the Fredrickson classification of abetalipoproteinemia?
Normal
90
What are the major risks associated with abetalipoproteinemia?
Fat-soluble vitamin deficiencies and neurological deficits
91
What is the genetic defect in analphalipoproteinemia (Tangier disease)?
Inability to synthesize apo A
92
What is the Fredrickson classification of analphalipoproteinemia?
Normal
93
What are the major risks associated with analphalipoproteinemia?
Neurological deficit and cholesterol ester storage in abnormal sites.
94
What are the functional groups in an LDL receptor protein?
Signal sequence, ligand-binding domain, EGF precursor homology region, O-linked sugar region, membrane-spanning domain, and cytoplasmic tail
95
What is an Alu sequence?
An Alu sequence is a short section of DNA, originally characterized by the action of Alu restriction endonuclease. They don't code for protein, but they are implicated in inherited disorders and cancers.
96
What is the function of ABC transporters?
The ABC transporters ABCA1 and ABCG1 are responsible for cholesterol efflux from peripheral tissues to HDLs circulating in the blood.
97
What are some causes of secondary hyperlipidaemia?
Type 2 DM, cholestatic liver disease, nephrotic syndrome, chronic renal failure, hypothyroidism, cigarette smoking, anorexia nervosa, obesity, beta blockers
98
What is xanthoma?
Xanthoma is caused by lipid deposits. It may indicate hyperlipidaemia, hypercholesterolaemia, heart disease or pancreatitis.
99
What is arcus senilis?
Arcus senilis is fatty deposit on the edge of the cornea.
100
What is metabolic syndrome/syndrome X?
Metabolic syndrome is a combination of disorders that increase the risk of developing cardiovascular disease or diabetes. It is defined by: central obesity and any 2 of: raised triglycerides, reduced HDL cholesterol, raised BP, raised fasting plasma glucose.
101
What are statins?
Statins inhibit cholesterol biosynthesis, they lower blood cholesterol. They are involved in inhibiting HMGCoA reductase.
102
State some non-statin cholesterol-reducing drugs.
Niacin, fibrates, CETP inhibitors, PCSK9 inhibitors

Biochemistry (3 decks)

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