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Clinical Chemistry > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

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1
Q

These provide the transportation system for different types of water insoluble fatty substances

A

Lipoproteins

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2
Q

How are fats absorbed from diet and lipids synthesized by liver and adipose tissues, transported in the aqueous blood plasma?

A

associating non-polar lipids (triacylglycerol and cholesterol esters) with amhipathic lipids (phospholipids and cholesterol) and proteins to make water-miscible proteins

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3
Q

How do lipoproteins mediate the production of water-miscible lipoproteins?

A

They transport lipids from the intestine as chylomicrons and from the liver as very low density lipoproteins (VLDL) to most tissues for oxidation and to adipose tissue for storage.

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4
Q

What happens to excess calories in humans?

A

ingested in anabolic phase of feeding cycle followed by negative caloric balance when organism draws upon its carbohydrates and fat stores

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5
Q

How is lipid mobilized from adipose tissue?

A

as free fatty acid attached to serum albumin

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6
Q

What is the purpose of lipoproteins?

A

transport hydrophobic lipid (fat) molecules in water, as in blood or extracellular fluid

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7
Q

What specifically comprises lipoproteins?

A

single layer phospholipid and cholesterol outer shell

*with non-polar core and single surface layer of amphipathic lipids

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8
Q

What consists the lipophilic or hydrophobic portions of each molecule?

A

Triacylglycerol and cholesteryl ester surrounded by a single surface layer of amphipathic phospholipids and cholesterol molecules

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9
Q

Lipoproteins may be separated according to what?

A

electrophoretic properties (alpha (-), beta (-) and pre beta (-) lipoproteins

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10
Q

T or F: the density of a lipoprotein decreases as the proportion of lipid to protein increases

A

true

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11
Q

types of lipoproteins

A

chylomicrons
very high density lipoproteins
low density lipoproteins
HDL

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12
Q

lipoprotein which is the biggest and derived from intestinal absorption of triacylglycerol and other lipids

A

Chylomicrons

primary concentration of fat that travel to different tissues

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13
Q

Chylomicrons are responsible for transport of what

A

dietary tryiglycerides (exogenous) from the GI tract to liver to skeletal muscle and to adipose tissue

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14
Q

Composition of chylomicrons

A

Phospholipids
Cholesterol at core
Triglycerides (90-95%)
Protein (added by liver; if fats arent attached to proteins, lipoproteins should be increased like apolipoprotein B)

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15
Q

What happens after eating high fat food?

A

fat is emulsified by pancreatic lipase, increasing the surface area for absorption through the enterocyte.
*intestinal lining contains receptors that absorb the esterified fat afte which, it goes to the blood then most of it goes to the liver

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16
Q

[Synthesis of chylomicrons]

1. -2. Where are lipid components assembled?

A

SER and golgi apparatus of mucosal cells with apoproteins (B-48 and A-apolipoprotein) synhesized in RER

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17
Q

[Synthesis of chylomicrons]

3. The assembled lipid components are called?

A

nascent chylomicrons

*exocytosed into the lacteals of the intestinal villi; appear only after meals rich in fats

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18
Q

[Synthesis of chylomicrons]

4. How do nascent chylomicrons reach general circulation?

A

from lymph vessels (lacteals) via thoracic duct

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19
Q

[Synthesis of chylomicrons]

5. When are dietary lipids incorporated in chylomicrons?

A

following absorption in intestine

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20
Q

[Metabolism of chylomicrons]
1-2. What do the initial chylomicrons (synthesized by intestinal cells and only contain apoB-48 and apo A) acquire upon entering circulation?

A

apo C-II and apo E from plasma HDL to form mature chylomicrons

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21
Q

[Metabolism of chylomicrons] 3-4. T or F: apo E activates the enzyme lipoprotein lipase which causes hydrolysis of about 80-90% of the chylomicron triacylglycerols in the peripheral tissue such as muscles and adipose tissue

A

False, apo C-II

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22
Q

[Metabolism of chylomicrons]

5. What accompanies hydrolysis of chylomicron triacylglycerols?

A

transfer of most of the A and C-apolipoproteins to HDL.

*changes convert chylomicrons into smaller particles (chylomicron remnants)

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23
Q

[Metabolism of chylomicrons]

7. What happens to the fatty acids and glycerol released from the hydrolyzed triacylglycerols

A

FA: enter muscle and adipose tissue cells
Glycerol: enters the liver where it is used for synthesis of TAG

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24
Q

[Metabolism of chylomicrons] What happens to chylomicron remnants?

A
  1. removed from blood circulation by liver
  2. bind to lipoprotein receptors on surface of hepatocytes
  3. whole remnant particle is taken by hepatocyte via endocytosis
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25
Q

[Fate of chylomicron remnants] What happens to intracellularly endocytosed vesicles?

A

carried to lysosomes where they are degraded to release the constituents

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26
Q

T or F: Chylomicrons are usually present in plasma after fasting

A

False, removed from plasma within 6 hours by liver (inadequate clearance = creamy layer on plasma)

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27
Q

VLDLs are secreted directly into the blood of liver as?

A

nascent VLDL particle containing Apo B-100 which obtain Apo C-II and Apo E from circulating HDL

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28
Q

VLDLs are used in transporting what?

*50-65% = triglyceride
can be from excess dietary carbs converted in liver

A

endogenous triglycerides from liver to tissues for storage energy and newly synthesized triglycerides from liver to adipose tissue

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29
Q

These are also known as B-Lipoproteins and the most atherogenic lipoproteins which represents a final stage in catabolism of VLDL

*50% = cholesterol

A

LDLs

  • transport cholesterol from liver to peripheral tissues
  • synthesized in liver
  • not in blood for long (need 12 hrs for test)
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30
Q

These lipoproteins are involved in VLDL and chylomicron metabolism and collect fat molecules from body’s cells/tissue to the liver

A

High Density Lipoproteins

  • also synth in liver (but also in intestine)
  • modulates VLDL in liver
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31
Q

T or F: HDLs work with VLDLS and LDLS to transport fat

A

false, VLDLs and chylomicrons

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32
Q

Why are HDLs considered as good cholesterol?

*30% phospholipids
20% cholesterol
50% apoprotein

A

→ More stable because it has more protein in membrane
→ Not easily absorbed in some parts of the body
→ Low triglyceride levels

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33
Q

Which apoproteins are good?

A

all except B (A, C others)

34
Q

Key lipids in lipoproteins

A

→ Cholesterol
→ Triglycerides
→ Phospholipids (Serves as protection)
→ Glycolipids

35
Q

Structure of the lipoprotein

A

→ Apoprotein
→ Cholesterol Esters (Found inside the lipoprotein)
→ Triacylglycerol (If LP is from liver)
→ Phospholipids
→ Free cholesterol
(creates closer interaction of the phospholipids and contributes to membrane stability)

36
Q

pathway wherein transport of dietary lipids, mostly the chylomicron
transportation of triglycerides to the liver.

A

exogenous pathway

37
Q

Transportation of lipids from the liver to the tissues (VLDL & LDL)

A

Endogenous Pathway

38
Q

What is considered as high and normal triglyceride levels?

A

High: >=500 mg/dL
Normal: <= 150 mg/dL

39
Q

[lipoprotein components] a glycerol with 3 attached fatty acids

A

triglyceride

*Exogenous source: Dietary
Endogenous source: Liver and Tissue storage
*95% of body fat (energy source)

40
Q

hormones which regulate triglyceride catabolism

A

lipase, epinephrine, cortisol

tri> mono

41
Q

lipoproteins which transport triglyceride

A

chylomicrons (exogenous)
VLDL (80% endogenous)
LDL (15% endogenous)

42
Q

these are short to long chained molecules which compose triglycerides

A

fatty acids

43
Q

Fatty acid which is SOLID at room temp

A

saturated fatty acids

*no double bond between carbons and from animal sources

44
Q

Sources of unsaturated fatty acids

*with double bonds between carbons and usually liquid at room temp

A

plant sources (palmitoleic acid, oleic acid, myristoleic acid, linoleic acid, and arachidonic acid)

45
Q

Why are most trans fatty acids bad?

A

synthetically made

without double bonds = blobs of fat
*some are good like palm oils

46
Q

Optimal range of cholesterol

*component of membranes: steroid hormones, bile and vit. D

A

100-129 mg/dL

47
Q

diseases which cause decrease in cholesterol below optimal levels

A

sphingomyelin problems

cerebrokinase deficiency

48
Q

T or F: bacteria and plants do not synthesize cholesterol

A

true

plants have phytosterols which are good and lessen cholesterol absorbed in system

49
Q

T or F: VLDL and chylomicrons transport cholesterol

A

false, HDL and LDL

50
Q

These are used to determine fetal lung maturity from amniotic fluid

A

lecithin and sphingomyelin (phospholipids)

51
Q

lipids with a carbohydrate content

A

glycolipids

*2/3 of glycolipids are distributed in intracellular membranes such as the golgi apparatus, endosomes, lysosomes, nuclear membrane, and mitochondria
•For cell to cell recognition and regulation

52
Q

How do substrates recognize cell (ABO incompatibility)

A

glycolipid moiety attached to phospholipid head

*used in signaling

53
Q

these are outer protein “shell” of lipoprotein molecule which binds together lipids for transport

A

apolipoprotein (B, C, E)

54
Q

biggest alipoprotein and primarily composes the VLDL

A

Apo B-100 (synthesized in the liver)

*one of the longst single polypeptide chains known

55
Q

truncated form of apo B synthesized in intestine which chylomicrons contain

A

B-48

*forme from same mRNA as B-100 after introduction of a stop signal by an RNA editing enzyme

56
Q

These are smaller polypeptides freely transferable between several different lipoproteins

A

Apo C-1, C-II, and C-III

57
Q

These are found in VLDL, HDL, chylomicrons, and chylomicron remnants

A

Apo-E

*accounts for 5-10% of total VLDL apolipoproteins in normal subjects

58
Q

What disease is influenced by different alleles of Apo E?

A

Alzheimer’s Disease (Dementia)

59
Q

What is Apo E responsible for?

  • Mainly produced by astrocytes
  • Transports cholesterol to neurons via Apo E receptor
A

interactions with cell membranes and enzymes to transport lipids to specific locations
(with role in immunity)

60
Q

apolipoprotein which is a cofactor of enzymes

A

→ Apo-AII and Apo-C-II for Lipoprotein Lipase
→ Apo-A-I for Lecithtin cholesterol acyl transferase or enzyme inhibitors
→ Apo C-I for cholesteryl ester transfer proteins

61
Q

apolipoprotein which is part of structure of lipoproteins

A

apo B

62
Q

Other functions of apolipoproteins

A

Ligands for interaction with lipoprotein receptors in tissues
→ ApoB-100 and apo E for the LDL receptors
→ apo E for the LDL receptor– related protein (LRP) which has been identified as the remnant receptor,
→ Apo A-1 for the HDL receptor.

63
Q

This is believed to be an important factor in human neuordegenerative disorders

A

Apo D

64
Q

apoprotein for activation of LPL

A

Apo C-II

65
Q

apoprotein which is a major structural protein of HDL and activator of LCAT

A

Apo A-1

66
Q

apoprotein which modulates hepatic uptake of VLDL and IDL

A

Apo C-1

67
Q

apoprotein which aids in secretion of VLDL from liver, a structural protein of VLDL, IDL and HDL and a ligand for LDLR

A

Apo B-100

68
Q

apoprotein which is an inhibitor of LPL activity

A

Apo C-III

69
Q

apoprotein which is a ligand for binding of IDL and remnants to LDLR and LRP

A

Apo E

70
Q

apoprotein aids in secretion of chylomicrons from intestine

A

Apo B-48

71
Q

effects of insulin

A

→ Always decreases plasma glucose
→ Inactivates lipase (Decreases lipolysis and the catabolism of triglycerides to fatty acids or glucose)
→ Stimulates lipogenesis (Involved in the conversion of fatty acid to triglycerides)
→ Allows transport of fat to the hepatocytes
→ Increase efficiency of gluconeogenesis

72
Q

What happens with insulin deficiency in DM cases?

A

insulin deficiency promotes the release of fatty acids via lipolysis of triglycerides by the liver (lose weight)

73
Q

Why are laboratory measurements of lipoproteins important?

A

association with coronary artery disease

74
Q

How many hours should a patient fast for total cholesterol and triglyceride testing?

A

at least 12 hours

75
Q

What enzymes do most methodologies in triglyceride testing use?

A

those that break glycerol from its fatty acids since triglyceride cannot be measured directly

76
Q

How is HDL testing done?

A

Dextran sulfate, a precipitating agent, is added to patient’s plasma wherein non-HDL is precipitated and centrifuged to bottom leaving supernatant to contain HDL to be measured via total cholesterol method.

77
Q

What can interfere with HDL testing?

A

Elevated triglycerides (>400mg/dL) may interfere with the separation of non- HDL (lower HDL)

78
Q

What equation is used to calculate LDL since direct measurement is uncommon?

A

Friedewald calculation
→ 𝑳𝑫𝑳 − 𝑪 = 𝑻𝒐𝒕𝒂𝒍 𝑪𝒉𝒐𝒍𝒆𝒔𝒕𝒆𝒓𝒐𝒍 − 𝑯𝑫𝑳 − 𝑻𝒓𝒊𝒈𝒍𝒚𝒄𝒆𝒓𝒊𝒅𝒆𝒔/ 𝟓
→ Example: Cholesterol= 200; HDL= 35; Triglyceride= 200
LDL= 125 mg/dl

79
Q

cholesterol deposits in coronary arteries occlude blood flow

A

arteriosclerosis

*heart (CAD)
arms/legs (PVD)
brain (CVD)

80
Q

conditions associated with plaque formation in Arteriosclerosis

A

→Increased plasma cholesterol
− Can also accompany increase in HDL if healthy diet is observed with fatty diet
→ Increased plasma LDL
→Decreased plasma HDL

81
Q

(see target ranges by NECP and other risk factors for CAD)

A

(see target ranges by NECP and other risk factors for CAD)

82
Q

plasma is placed inside the donut where lipids spin to the outside of donut

A

ultracentrifuge

Clinical Chemistry (9 decks)

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