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Fundamentals of the Living Cell > Lipid Transport > Flashcards

Lipid Transport Flashcards

1
Q

describe the properties of FFA

A
  • formed from triglycerides stored in adipose tissue
  • circulates bound to Na+ salt particularly the albumin protein
  • saturation at 2mM of FA molecules
  • enters cells by simple diffusion
  • intracellular [FA] kept low
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2
Q

why do FFA need to travel bound to proteins?

A

if unbound they will act as detergents

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3
Q

what is a lipoprotein?

A

biochemical assembly whose purpose is to transport hydrophobic lipid molecules in water, blood, extracellular fluid

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4
Q

what is the structure of a lipoprotein?

A
  • membrane consists of phospholipids and cholesterol and large apolipoproteins
  • in centre, there are cholesterol esters and triacylglycerol
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5
Q

what are the 5 lipoproteins?

A
  • chylomicrons
  • very low density lipoproteins (VLDL)
  • intermediate density lipoproteins (IDL)
  • low density lipoproteins (LDL)
  • high density lipoproteins (HDL)
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6
Q

what are the compositions of the 5 lipoproteins?

A

-comp varies between diff lipoproteins

  • CHYLOMICRONS: most (90-95%) triglycerides, so the least dense
  • VLDLs: mostly triglycerides (53%)
  • LDLs: mostly (50%) cholesterol
  • IDLs: intermediate in all (highest is triglycerides, 31%)
  • HDLs: mostly (49%) protein
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7
Q

what are apoproteins/apolipoproteins?

A

proteins that bind lipids together to form lipoproteins

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8
Q

what are the functions of apoproteins?

A
  • structure
  • solubilise lipids
  • act as enzymes or enzyme cofactors
  • tissue targeting
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9
Q

what is an example of apoproteins acting as enzymes or enzyme cofactors?

A
  • APO C2 activated lipoprotein lipase (breaks down fat in form of triglycerides)
  • APO A1 activates lecithin-cholesterol acyl transferase (converts free cholesterol into cholesteryl esters)
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10
Q

what is an example of apoproteins involved in tissue targeting?

A
  • APO B100 and APO E bind to the LDL receptor

- APO E binds to the HDL receptor

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11
Q

how does the synthesis of chylomicrons happen?

A
  • forms in the cells that line the gut
  • in lumen of gut, triglycerides broken down into FA
  • FA and monoglycerides brought into mucosal cell where they are reformed into triglycerides
  • they are combined with other lipids proteins to form chylomicrons
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12
Q

how and why are chylomicrons delivered directly into the lymph system?

A
  • secreted into lymphatics which carries them via thoracic duct into superior vena cava
  • dietary fats avoid direct delivery to liver and made available to the extra hepatic tissue
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13
Q

where are digested proteins and carbohydrates delivered?

A

released into portal vein and delivered directly into liver

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14
Q

how does a nascent chylomicron become a mature chylomicrons?

A

nascent chylomicron interacts w HDL and pick up certain apoproteins

-occurs in SER

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15
Q

what are chylomicrons for and how are they removed?

A
  • important for transporting exogenous dietary lipids from gut around circulation
  • they reflect meal composition
  • remnants are removed by liver
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16
Q

what do chylomicrons contain and what is their lifeline?

A
  • contains fat soluble vitamins like vit A and e

- lifetime in circulation is 1 hour

17
Q

why doe chylomicrons have a low density?

A

due to high [triglyceride]

18
Q

how does lipoprotein lipase work?

A
  • LPLs bind to and activated by APO C2

- lipoprotein binds to LDL and triglycerides pithing are degraded

19
Q

where are LPLs found?

A

vary with tissue, found in cells that use a lot of fats

20
Q

what is hyperlipidaemia?

A

abnormally elevated levels of any/all lipids or lipoproteins in the blood

21
Q

what are the different types of hyperlipiaemia?

A
  • T1: caused by deficiency in LPL or APO C2
  • T2: high LDL
  • T4L: most common: increased VLDL due to obesity and alcohol abuse
22
Q

what are VLDLs and what are they metabolised by?

A
  • responsible for transporting endogenously-synthesis lipids

- metabolised by LPL as they circulate

23
Q

what is VLDL halflife nad what is their formation enhanced by?

A
  • HL: 15-60mins

- enhanced by dietary intake of carbs, circulating FFAa, alcohol, raised insulin, decreased glucagon

24
Q

how does VLDL convert in mature VLDL and where is it synthesised?

A
  • synthesised in liver, ER, GA
  • when released as nascent VLDLs, they only have APO B100 apoprotein

-when they interact w HDL, HDL donates APO C2 and APO E making it mature

25
Q

what are the 2 fates of VLDLs?

A
  • when lost majority of triglyceridesm remnants return to liver or converted to IDLs
  • converted to LDLs which will be removed by liver and non-hepatic tissue for steroid biosynthesis
26
Q

what are the functions of LDLs?

A
  • major carriers of cholesterol
  • metabolised slowly (3 days)
  • catty cholesterol to periphery and regulate denovo synthesis of cholesterol
  • has APO B100 so can bind to receptor on hepatocytes
27
Q

what are the 3 ways HDLs are made?

A
  • as nascent HDLs in liver nad intestine
  • budding from VLDLs and chylomicrons
  • from free APO A1
28
Q

how do HDLs remove cholesterol from circulation?

A
  • contain enzyme lecithin-cholesterol acyltranferase (LCAT)
  • LCAT modifies free cholesterol and retains it within HDL
  • prevents cholesterol from diffusing out of HDL
29
Q

how does HDL pick up cholesterol?

A
  • reverse cholesterol transport
  • occurs in plasma and endothelial cells
  • they express ABCA1 transporter which moves cholesterol from extracellular surface of membrane and interacts w APO A1 on HDLs to transport cholesterol away
30
Q

what is the significance of the HDL/LDL ratio and what is the normal ratio?

A
  • HDL referred to good cholesterol dn LDL as bad
  • ratio used to asses susceptibility to heart disease

-normal is 3.5

31
Q

how are lipoproteins removed from circulation?

A

removed by receipt mediated endocytosis

32
Q

describe the receptor mediated endocytosis in relation to LDLs

A
  • LDLs bind to specific LDL receptor on endothelial cells
  • cause for the invagination of LDL and receptor which forms an endoscope
  • in endoscope, receptor nad LDL dissociate so receptor can be recycled
  • LDL broken down by fusion of lysosome with endosome
  • cholesterol esters converted to cholesterol where they are immediately esterified
  • triglycerides broken down to give FA which can be further metabolised into aa
33
Q

how is receptor mediate endocytosis regulated?

A

-regulated by intracellular [cholesterol]
-which regulates expression of new and existing receptors on membrane
-witj increased cholesterol, HMG-CoA reductase energy inhibited
-

34
Q

what is an example of when there is a loss of LDL receptor function?

A

-familial hypercholesterolemia

  • loss of LDL receptor function
  • 4x the normal cholesterol serum levels
  • develop blocked arteries
  • tend to die young from heart attacks
  • de novo synthesis not regulated by LDL
  • single aa substitution prevents localisation of LDL receptor to coated pits
35
Q

what are the 2 types of receptors and where are they present?

A
  • high affinity LDL receptor
  • low affinity scavenger receptor
  • present on endothelial cells, macrophages, vascular smooth muscle cells
  • low affinity scavenger receptors activated when plasma LDL levels high or when chemically modified
36
Q

what are 3 situations where there are abnormalities in lipid transport?

A
  • diabetes mellitus: increased [FA] mobilisation, decreased [LDL]
  • obesity: can cause hypertension, hyperglycaemia, hypoglycaemia
  • gene defects of proteins: leads to hypercholesterilemia, atherosclerosis
37
Q

where do chylomicrons transport fat?

A

small intestine to capillaries

38
Q

where do IDL and LDL transport fat?

A

capillaries to extra hepatic tissue

39
Q

where does HDL transport fat?

A

extra hepatic tissue to liver

Fundamentals of the Living Cell (31 decks)

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