Transport of fats Flashcards

1
Q

What are the general components of a lipoprotein?

A

The shell is made of apoproteins, phospholipids, and unesterified cholesterol

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2
Q

What is the general change in composition of lipoproteins as they increase in density?

A

They tend to become smaller; and have increased levels of cholesterol and protein relative to triacylglycerides

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3
Q

Where are the ApoB-48 proteins found and what is the difference between it and the ApoB-100?

A

They exist mainly on chylomicrons; their RNA transcripts are edited to introduce a stop codon that eliminates the LDL receptor binding region

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4
Q

Which lipoproteins have ApoB-100 on their surfaces?

A

VLDL, IDL, and LDL

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5
Q

What is the role of lipoprotein lipase? Where is it found?

A

It exists on capillary endothelium of muscle cells, adipose tissue and active mammary gland cells; when activated by Apo-CII, it will release fatty acids from TAGs and absorb them

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6
Q

What is the role of ACAT?

A

It esterifies cholesterol that comes into cells from the lipoproteins

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7
Q

What is the role of LCAT?

A

It is found on HDLs and converts cholesterol remnants in chylomicrons and VLDL to cholesterol esters for transport. Needs ApoA-1

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8
Q

What is the role of CETP?

A

It will transfer TAG and cholesterols between lipoproteins

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9
Q

What is the transport role of chylomicrons?

A

They ferry TAGs to adipocytes

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10
Q

What is the transport role of VLDL and LDL?

A

They ferry TAGs and cholesterol respectively from the liver to the peripheral tissues

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11
Q

What is the transport role of HDLs?

A

They will ferry excess cholesterol from the periphery to the liver

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12
Q

What are the main apoproteins on chylomicrons?

A

ApoB-48, ApoE, ApoC-II

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13
Q

What apoproteins are commonly found on VLDL, IDL, and LDL?

A

ApoB-100, ApoC-II (VLDL and IDL have Apo-E)

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14
Q

How do VLDLs become converted to other types of carriers?

A

As they lose their fatty acids, they gain density and become IDLs; as IDL lose their ApoE proteins they become LDLs

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15
Q

How are LDLs processed by peripheral cells?

A

Instead of taking fatty acids out of the lipoprotein, the cell engulfs the whole packed through the LDL receptor and conjugates the cholesterol components with oleic acid

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16
Q

How does familial hypercholesterolemia occur?

A

Genetic mutations in the LDL receptors prevent the individual from absorbing LDLs

17
Q

How do HDLs morphologically change over the course of their jobs?

A

They start out discoid when they are empty and as they fill they become spheroid

18
Q

How do HDLs lose their acquired cholesterols?

A

They bind to the SR-B1 receptor on the liver surface and cholesterol is extracted

19
Q

How the LDLreceptor gene regulated?

A

The SREBP system also controls transcription of the receptor; if cholesterol levels in the cell are high, then the receptor will be downregulated

20
Q

What percentage of bile salts are recycled daily?

A

95%; the 5% that is excreted is the body’s main way of eliminating cholesterol

21
Q

How is cholesterol converted to a bile salt?

A

A cytochrome P-450 enzyme, cholesterol-7-alpha-hydroxylase uses oxygen to introduce polarity to cholesterol.

22
Q

How are bile acids conjugated?

A

They are transformed to strong acids by addiition of glycine or taurine to the carboxylic acid region of the bile acid

23
Q

How is bile salt synthesis regulated?

A

High serum cholesterol levels promote upregulation of the 7-alpha-hydroxylase; high bile salt levels inhibit transcription

24
Q

What are desired, borderline, and high levels of serum cholesterol?

A

Desired is less than 190 mg/dL; borderline is 200-240 mg/dL; High is in excess of 240 mg/dL

25
Q

What are optimal targets for LDL and HDL levels?

A

LDL levels should be 100-129 mg/dL; HDL levels should be around 50 mg/dL

26
Q

How can ApoE be correlative with Alzheimer’s risk?

A

Patients who are homozygous for the E4 variant have a much higher risk of developing late onset Alzheimers