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CVS Biochemistry > Cholesterol & Lipoprotein Metabolism > Flashcards

Cholesterol & Lipoprotein Metabolism Flashcards

1
Q

Cholesterol is …C, made of … rings, it has an 8C chain attached to …., -OH is attached to …. There is double bond between …..

A 
27
4
C17
C-3
C5 & C6
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2
Q

Mention importance of cholesterol

A

Structural components of cell membrane, modulating their fluidity
Cholesterol is a precursor of bile acids, steroid hormones & vit D

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3
Q

HDL is used to …. While LDL is used to …..

A

Transport cholesterol from body tissue to cells

Transport CE from liver to body cells

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4
Q

Mention cells which can effectively excrete CE

A

Hepatocytes

Enterocytes

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5
Q

Mention the major sterol in stool

A

Coprostanol

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6
Q

CE synthesis requires ….&… Carbon atoms are provided by ……

A

NADPH & ATP

Acetyl CoA

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7
Q

Mention sites of enzymes required for CE synthesis

A

Cytosol

Membrane Of SER

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8
Q

….. enzyme condesnsed 2 acetyl CoA nolecules & ….. adds a third one forming ….

A

Thiolase
HMG CoA synthase
HMG CoA

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9
Q

Describe HMG CoA reductase reaction

A

Reduce HMG CoA to mevaonate using two molecules of NADPH & CoA is released. It is the rate-limiting step.

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10
Q

Mevalonate is converted to …. Then to …..by… then to ….

A

Isoprene
Squalene by cindensation
Lasosterol

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11
Q

….&….. feedback inhibit HMG CoA reductase

A

Mevalonate

IC cholesterol

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12
Q

What is the effect of defective cellular LDL receptor

A

Dec IC cholesterol level, dec feedback inhibition of feedbck inhibition, so there is inc of cholesterol blood level with continuous IC synthesis of cholesterol.

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13
Q

Describe covalent regulation if HMG CoA reductase

A

It is active in dephosphorylqted form by phosphatase (stimulqted by insulin)
It is inactive by phosphorylation by AMP kinase which itself is activated by a kinase (glucagon and epinepherine activate AMPK by inc cAMP)
AMPK is inactivated by dephosphorylation by phophqtase stimulated by insulin

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14
Q

What happens when sterol levels in scell are low?

A

The SREBP-SCAP complex is released from ER to Golgi where it is cleaved into a soluble fragment, that enters the nucleus and acts as transcription factor at SRE and inc HMG CoA reductase synthesis leading to inc cholesterol synthesis.

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15
Q

….. are proteins shown to inhibit exit of SCAP/SREBO compkex from ER to Golgi.

A

Insigs

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16
Q

Mention hormones which inc and dec HMG CoA reductase

A

I, inuslin & thyroxine

D, glucagon & glucocorticoids

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17
Q

Describe sterol accelerated enzyme degradation

A

The reductase itself is sterol sensing, when cholesterol level inc it binds to insigs leading to ubiquitation & proteasomal degradation.

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18
Q

GR, Statins cause myopathy

A

Their inhibition if HMG CoA reductase leads to lessening of downstream synthesis of CoQ (part of ETC) leading to dyfunctional mitochobdria and decreased ability to generate ATP for muscle contraction.

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19
Q

…..catalize esterification of CE

A

Cholesterol acyl transferase

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20
Q

….acts within cells, ….acts within HDL (for cholesterol esterification)

A

Acetyl CoA CAT

Lecithin CAT

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21
Q

Mention importance of LCAT in HDL & LCAT activity is associated with ….protein

A

Creates a gradient for transport of choelsterol from tissue to HDL
Apo A1

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22
Q

GR: Obstructive jaundice causes hypercholesterolemia

A

Due to blocked bioe secretion (which dec CE excretion) & cholestasis which dec conversion of CE to bile.

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23
Q

GR: Hypothyroidism causes hypercholesterolemia

A

Due to dec expression of LDL receptor leading to dec LDL-C uptake (although HMG CoA reductase activity is reduced)

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24
Q

GR: DM causes hypercholesterolemia

A

Inc level of FA oxidation, inc acetyl CoA, inc CE synthesis

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25
Q

GR:Nephrotic syndrome causes hypercholesterolemia

A

Due to loss of liporegulatory proteins in urine HDL, LCAT, Apo CII

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26
Q

Decribe effect of estrogen on CE

A

It induces HDL & Apo A1 synthesis also in LDL receptors thus enhances LDL catabolism

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27
Q

GR: Hyperthyroidism causes hypocholesterolemia

A

Due to increased expression of LDL receptor resulting in inc LDL receptor mediated catabolism of LDL particles

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28
Q

Nascent HDL shape is

A

Discoidal

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29
Q

FFA are carried in blood bound to …

A

Albumin

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30
Q

Hydrophobic core of lipoproteins contains ……, while hydrophilic coat contains ……

A

TAG +Cholesterol ester

Cholesterol + PL + apoprotein

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31
Q

Mention the Pripheral Apoproteins

A
  1. Apo A I, II & IV
  2. Apo C I, II & III
  3. Apo D
  4. Apo E
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32
Q

Describe the functions of palsma apoprotiens

A

Structural: stabilize & maintain the molecular structure of the molecule
Regulatory: serve as cofactors for enzymes Apo A1 activates LCAT, Apo CII activates lipoprotein lipase
Ligands: for lipoprotein interactions with receptors Apo B100 for LDL, Apo E for CM, Apo A1 for HDL ALL IN LIVER BUT LDL IS ALSO EXTRAHEP

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33
Q

Mention the apoproteins which freely transferrable between different plasma lipoproteins

A

Apo CI, CII

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34
Q

GR: Although Apo B48 & B100 are from the same gene they are different

A

Due to introducing of a stop signal by mRNA editing enzyme in the intestine allowing translation of 48% of Apo B100 (pot-transcriptional modification)

35
Q

Mention the lipoprotein with least density

A

Chylomicron

36
Q

Arrange from cathode to anode lipoproteins in electrophoresis

A 
Chylomicron (origin)
Beta lipoprotein (LDL)
Broad beta lipoprotein (IDL)
Prea-beta lipoprotein (VLDL)
Alpha lipoprotein (HDL)
37
Q

Functions of lipoproteins

A

Transport of exogenous & endogenous lipids
Transport of fat soluble vits
Transport of fat soluble drugs
Delivery of cholesterol to steroid hormones producing tissue

38
Q

Describe the lipid transport function of lipoproteins

A
  • CM transports TG from intestine to liver & tissues
  • VLDL transports TG from liver to extrahep tissue
  • LDL carries chol from liver to extrahep tissue
  • HDL carries chol from peripheral tissues to liver
39
Q

Mention function & site of LPL

A

Hydrolyze TAG in VLDL & CM relaesing FFA & glycerol
It is an extracellular enzyme anchored by heparan sulphate to the capillary wall of most tissues (cardiac & skeletal muscle tissue & adipose tissue but no adult liver) & lactating mammary glands.

40
Q

What are cofactors of LPL

A

Apo CII

Phospholipids

41
Q

GR: Adipose cells gain fat in well-fed state

A

As Insulin enhance LPL synthesis in adipocytes

42
Q

LCAT is formed by ….., it is activated by ……, associated with ….. .

A

Liver
Apo A
HDL

43
Q

Describe reaction catalyzed by LCAT

A

Lecithin + cholesterol —> CE + Lysolecithin

44
Q

What is the func of hepatic lipase

A

Continues lipolysis of IDLs in the stepwise coversion to LDL also hydrolyese HDL-TAGs.

45
Q

CM are synthesized in …., …. Is unique to them.

A

Intestinal mucosal cells

Apo B48

46
Q

…&…. Are added to nascent CM to become mature

A

Apo CII & Apo E

47
Q

Glycerol in the liver is used for…,…&…

A

Lipid synthesis, glycolysis & glucogenolysis

48
Q

Compare Km of LPL in adipose tissue & heart

A

A.t., high Km

H, low Km

49
Q

GR: LPL acivity is inc in mammary glands in lactation

A

Because FFAs are released for milk synthesis

50
Q

…. Is reteurned to HDL from CM

A

Apo CII

51
Q

GR: Plasma becomes turbid after a fatty meal

A

Due to high level of nascent CM

52
Q

LPL is also called ….factor

A

Clearing

53
Q

….% of TAG in VLDL is endogenous

A

60

54
Q

…… are transferred from VLDL to HDL, while …. are transferred from HDL to VLDL by action of ….

A

TAG
Cholesteryl esters
Cholesteryl ester transfer protein (Apo D)

55
Q

Mention surface component(s) lost from VLDL to become LDL

A

Apo C & some apo E

56
Q

IDL could be taken up by receptor mediated endoctosis though

A

Apo E

57
Q

LDL receptors are ….. charged ……. that are clustered in ….. on cell membrane, that is coated from cytosolic side by …..

A

Negatively
Glycoproteins
Pits
Clatahrin

58
Q

Mention effects if endocytosed cholesterol on IC homeostasis

A

1st, HMG CoA reductase is inhibited by high cholesterol
2nd, synthesis of new LDL receptor protein is reduced by decreasing the expression of LDL receptor gene (by hormone response element) so LDL entry is limited
3rd if cholesterol is not urgently needed: it is stores as CE by ACAT enzyme, synthesis of steroids in adrenal cortex & gonads, enter cell membrane efflux to HDL by LCAT

59
Q

Write a short note on uptake of chemically modified LDL by scavanger receptor A

A

The receptor in found on endothelium of blood vessels & macrophages.
It binds with LDL in which the lipid on Apo B have been oxidized
Thus macrophages accumulate cholesterol causing transformation to foam cells, which from atherosclerotic plaque
The receptor is non-specific & unregulated

60
Q

What is the composition of Lipoprotein (a)

A

LDL + Apo (a)

61
Q

GR: LP (a) interferes with plasmiogen & what is the result?

A

Due to simlilarity between LP (a) & it interferes with tPA in fibrinolysis which can provoke the formation of acute thrombosis.

62
Q

Mention major functions of HDL

A
  1. Reservoir of apolipoproteins
  2. Uptake of unersterfied cholesterol
  3. Exterification & reverse transport of cholesterol
63
Q

Describe the LCAT reaction

A

Plasma enzyme activated by Apo A1
Transfers fatty acid from C2 of phosphatidylcholine to cholesterol forming hydrophobic CE, and lysophophatidylcholine binds to albumin.

64
Q

As nascent HDL accumulates CE it becomes ….., while when that process reaches max it is called ….

A

HDL3

HDL2

65
Q

Decsribe uptake of HDL by Liver

A

Teh mature spherical HDL2 return to liver to unload its cholesterol via Apo A1 & SR-B, tpwhich selectively uptake CE & release lipid depleted HDL3 which recirculates to extract lipids from lipoproteins in peripheral tissue.

66
Q

What is the importance of CTEP (chol ester transfer protein)

A

It relieves the product inhibition of LCAT by CE

67
Q

Write a short note on hyperlipoproteinemia type 1

A 
Deficiency of LPL or Apo CII
Chylomicronemia
Fasting hypertriacylglycerolemia
Craemy white plasma
No inc cholesterol or inc risk of coronary disease
68
Q

Write a short note on hyperlipoproteinemia type IIa

A

Due to defective LDL receptor or defective ApoB gene leading to elevated cholesterol, premature atherosclerosis inc risk for early onset ischemic heart disease. Associated with tendon xanthomas on hands & feet.

69
Q

Mention classes of LDL-receptors defects

A

No receptors
Receptor doesn’t bind to LDL normally
Receptor doesn’t accumulate on clatharin coated pit
Receptor doesn’t release LDL after internalization & does not recycle to cell surface

70
Q

Write a short note on secondary combined familial hyperlipoproteinena

A

Increased VLDL & IDL due to inc availability of substrates acetyl CoA, triglycerides & inc ApoB100 synthesis with dec LDL clearance so TAG & cholesterol are elevated. Usually in context of metabolic syndrome

71
Q

Mention metabolic risk factors

A
  1. Abdominal obesity
  2. Low HDL
  3. High triglycerides
  4. High BP
  5. High fasting blood sugar
72
Q

Write a note on type III hyperlipodproteinemia

A

Dysbetaliproteinemia, due to defective ApoE leading to high CM remnants & IDL result in elevated cholesterol & TAG.

73
Q

Write a note on type IV hyperliproteinemia

A

Hypertriglyceridemia, associated with obesity & DM T2, inc VLDL

74
Q

Write a note on type V hyperliproteinemia

A

It is silimar to type I with elevated VLDL in addition to CM associated with glucose intolerance thus dec in LPL which is insulin dependant & inc TAG & cholesterol.

75
Q

What is Tangier disease

A

A rare genetic disease characterized by near absence of HDL & Apo A1, leading to orange color tonsils, heptaosplenomegaly, premature premature CAD.

76
Q

GR: PUFA decrease risk of atherosclerosis

A

Because it inc the solubility of cholesterol

77
Q

GR: sucrose & fructose increase risk of atherosclerosis

A

Tend to stimulate synthesis of TAG, atherogenic.

78
Q

Decsribe effect of Caffiene on atherosclerosis

A

Inhibits phosphodiesterase so inc activity of hormone sensitive lipase, inc FFA & Lipoproteins

79
Q

Decsribe effect of smoking on atherosclerosis

A

Inc catecholeamines which inc adenyl cyclase activity and inc HSL activity inc lipolysis & inc FFA & lipoproteins. Smoking oxidizes LDL & leads to endothelial injury, also compromises body antioxidant vitamins status esp vit C.

80
Q

Decsribe effect of alcohol on atherosclerosis

A

Alcohol is oxidized to acetaldehyde which produces NADH and inc NADH/NAD ratio which favours conversion of DHAP to GAP & glycerolipids.

81
Q

GR: Water-soluble fibers prevent atherosclerosis

A

Through its ability ti reduce the amount of bile absorbed from the intestine

82
Q

GR: plant sterols prevent atherosclerosis

A

They look a lot like cholesterol, so when they travel through the digestive tract they block absorption of cholesterol

83
Q

GR: Vit E prevent atherosclerosis

A

Protects LDL & membrane lipid from oxidation

CVS Biochemistry (3 decks)

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