Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochem + Metabolism > Lipoproteins > Flashcards

Lipoproteins Flashcards

1
Q

How are long chained fatty acids transported in blood?

A

bound to ALB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the source of most circulating FFA?

A

mostly long chained fatty acids from hydrolysis of TG in adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How to medium chained fatty acids exist in blood?

A

bound to ALB or free

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How to short chained fatty acids exist in blood?

A

free

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the main source of short chained fatty acids?

A

mostly from fermentation by colonic or rumen bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why do free fatty acids in blood have low circulating concentrations/short half lives?

A

because, in health, there is rapid uptake by target tissues to use for energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When would you find high levels of FFA? decreased?

A

increased: starvation/fasting
decreased: post prandial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how many FFA can ALB carry at one time?

A

7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main target organs of FFA?

A

liver, kidney, heart, skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe FFA uptake at tissues

A

-enter cells via fatty acid transporters
-once inside, bound to cystolic fatty acid binding proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two potential fates of free fatty acids once inside target tissue cells?

A

-oxidation to produce energy or to synthesize ketone bodies from resulting acetyl CoA
-re-esterification to TG for storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 4 main molecules transported by lipoproteins?

A

-TG
-Phospholipids
-cholesterol
-cholesterol esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 4 main lipoproteins?

A

-CM
-VLDL
-LDL
-HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an apolipoprotein?

A

it is the protein component of lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between peripheral and integral apolipoproteins?

A

peripheral: can be exchanged between lipoproteins
integral: can not be exchanged, it helps define the lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two integral apolipoproteins?

A

A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the two apolipoprotein B isoforms? describe their function

A

B48: synthesized in the intestine and specific to CM
B100: synthesized in the liver, component of lipoproteins originating in the liver, VLDL IDL LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two A apolipoprotein isoforms? what lipoprotein are they integral to?

A

ApoA-1 is integral to HDL
ApoA-s are peripheral for CM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two peripheral apolipoproteins?

A

C and E

20
Q

Why is ApoCII important?

A

it is a cofactor for lipoprotein lipase and this stimulates TG hydrolysis

21
Q

Review: Describe lipid digestion

A

-Pancreatic lipases hydrolyzes TG into FFA plus monoglycerides
-Bile acids/salts enable formation of mixed micelles
-micelles travel to enterocyte membrane
-within jejunal cells TG are resynthesized and packaged into CM
-CM exit the intestine via lymphatics and enter general circulation

22
Q

Where are CM made?

A

only in the intestine

23
Q

How are CM remnants (after offloading) cleared from circulation?

A

they are cleared by the liver

24
Q

CM remnants have a higher percentage of what molecules as opposed to the original CM?

A

they have a higher percentage of cholesterol and cholesterol esters

25
Q

What two lipoproteins carry triglycerides?

A

CM and VLDL

26
Q

What are the roles respectively of the two TG carrying lipoproteins?

A

CM: carry TGs from the intestine
VLDL: carry TGs from the liver

27
Q

What is the purpose of VLDL?

A

carry TG from the liver to target tissues (adipose or muscle/heart depending on fed state)

28
Q

How are TGs taken up by target tissues?

A

-target tissues contain lipoprotein lipases
-LPL hydrolyzes TG in CM and VLDL to release free fatty acids to tissues
-CM remnants and IDL result which are ultimately cleared by the liver
-FFA are transported across the membrane into the cells

29
Q

Where in the cell is LPL?

A

attached to the endothelium lining adjacent blood capillaries of adipose, muscle and heart tissues

30
Q

How is LPL regulated by insulin?

A

Insulin increases LPL activity

31
Q

Why do you see hyperlipidemia in poorly controlled diabetics?

A

Because LPL activity is decreased which can lead to TG remaining in circulation

32
Q

Serum lipemia is caused by high levels of what?

A

TG

33
Q

From what is LDL derived?

A

from VLDL in the blood

34
Q

What is the main function of LDL?

A

cholesterol delivery to tissues

35
Q

What is the function of LDL receptors?

A

cell surface receptor that mediates the endocytosis of LDL

36
Q

What do LDL receptors recognize on LDL?

A

Apo-B100 and Apo- E

37
Q

True/False: all cells have LDL receptors?

A

true

38
Q

How is LDL cleared?

A

70% is cleared by the liver, 30% is degraded in extra hepatic tissues

39
Q

How are LDL- R regulated?

A

-transcription is inhibited by intracellular cholesterol concentration
-transcription is increased by thyroid hormone and insulin

40
Q

How are cholesterol levels regulated?

A

-increased dietary cholesterol inhibits de novo synthesis
-low dietary cholesterol leads to increased de novo synthesis
- LDL derived cholesterol regulates synthesis via HMG-CoA reductase. increased levels inhibits HMG-CoA reductase

41
Q

where is HDL synthesized?

A

the liver and some small intestine

42
Q

What is the function of HDL?

A

-uptake of free cholesterol
-cholesterol esterification by LCAT
-transport cholesterol to the liver to be excreted in bile

43
Q

Describe the structure and structural change of HDL

A

-newly formed HDL is discoid shape
-become spherical and expands as it collects cholesterol and other lipids

44
Q

What is hyperlipidemia?

A

high blood levels of TG and/or cholesterol

45
Q

true/false: post prandial hypertriglyceridemia or hypercholesterolemia is not normal

A

false

46
Q

What are the two primary causes of hyperlipidemia?

A

-post prandial
-idopathic

47
Q

What are the 6 secondary causes of hyperlipidemia?

A

-Diabetes mellitus
-hypothyroidism
-hyperadrenocorticism (cushings)
-pancreatitis
-cholestasis
-protein losing nephropathy

Biochem + Metabolism (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions