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Body Systems > Post absorption processing of lipids > Flashcards

Post absorption processing of lipids Flashcards

1
Q

what are some roles of fats

A

energy store
incorporation into the cell membrane (phospholipids and cholesterol)
precursors for prostaglandins, leukotrienes and thromboxane

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2
Q

what are the 4 uses of cholesterol

A

bile salts
membranes
vit D
steroid hormones

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3
Q

name 5 steroid hormones

A 
androgens (testosterone) 
oestrogens
progesterones 
mineralocorticoids (aldosterone) 
glucocorticoids (cortisol)
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4
Q

what are the real names of w-3 and w-6

A 
linoleic acid (6)
DHA/EPA (3)
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5
Q

what is the role of w-3 and w-6

A

fatty acids are precursors for both inflammatory and anti-inflammatory molecules

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6
Q

describe the pathway of turning linoleic acid (w-6) into arachidonic acid

A

linoleic acid
y-linoleic acid (GLA)
dihomo-y-linoleic acid (DGLA)
arachidonic acid

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7
Q

what can DGLA turn into

A

1-series
prostaglandins
thromboxanes

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8
Q

what can AA turn into and what affects does aspirin have

A

aspirin increases turning AA into lipoxins
aspirin decreases 2-series prostaglandins and thromboxane
can also turn into 4-series leukotrienes

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9
Q

what can DHA/EPA (w3) turn into and what affect does aspirin have on it

A

3-series protoglandins and thromboxanes
aspirin increases turning into protectins and resolvins
5-series leukotrienes

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10
Q

what are chylomicrons and how do they enter the subclavian vein

A

produced from lipids in diet
formed in intestinal epithelial cells and release into the lymph
enter circulation via thoracic duct and into the subclavian vein

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11
Q

do chylomicrons pass from GI tract to liver

A

no

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12
Q

what are the two ways in which fatty acts arrive at peripheral tissue

A

in chylomicrons or VLDL

from adipose tissue

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13
Q

what releases fatty acids from chylomicrons and VLDLs in peripheral tissue

A

lipoprotein lipase

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14
Q

how do fatty acids get to adipose tissue

A

triaglycerols broken down by hormone sensitive lipase
fatty acids released into blood
transported to tissues bound to albumin

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15
Q

does he brain receive fatty acids

A

no as fatty acids can’t cross the blood brain barrier

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16
Q

describe the process of oxidation of fatty acids

A

activation to fatty acyl CoA in cytosol
First step requires energy – ATP to AMP – priming step (cf glycolysis – phosphorylation)) – attached to CoA
This occurs in cytosol, then FA-CoA needs to be transported into mitochondria
If over 12C use carnitine transport –

3 steps – FA CoA released from CoA, attached to carnitine. Occurs on outer mit memb
Fatty acyl carnitine transferred across inner mit memb by carnitine acylcarnitine translocase – FA-carnitine transported in exchange for free carnitine
FA transferred back to CoA
This transfer is a controlled step – malonyl CoA is early metabolite in FA synthesis pathway – so prevents cycling

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17
Q

what is the specific role of carnitine

A

transports fatty acids across the inner mitochondrial membrane

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18
Q

describe the process of B oxidation of fatty acids

A

spiral process

each turn releases 1 acetyl CoA producing NADH and FADH2

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19
Q

what happens to the products of the B oxidation of fatty acid

A

NADh and FADH2 are oxidised in the electron transport chain

acetyl CoA enters the krebs cycle producing more NADH

20
Q

what is the overall product of the B oxidation of fatty acids and what type of process is this

A

108 ATP from each molecule of palmitoyl CoA

completely aerobic

21
Q

what produces more ATP oxidation of glucose or b oxidation of palmitoyl CoA

A

36 from oxidation of glucose but 108 from the other but this is totally dependant on oxygen

22
Q

how is b oxidation controlled

A

regulated by amount of fatty acids present in the mitochondria which is controlled by the concentration of malonyl CoA
ie regulation of substrate availability

23
Q

how is malonyl CoA produced

A

formed y acetyl CoA carboxylase in first step of fatty acid synthesis

24
Q

what inhibits carnitine acyl-transferase-1

A

high concentrations of malonyl CoA

25
Q

what are ketone bodies formed from and where does this process occur

A

excess acetyl CoA

mitochondria of liver cells under fasting or uncontrolled diabetes

26
Q

what are ketone bodies used for

A

released into the blood and are oxidised to produce energy in peripheral tissues including the brain tissue

27
Q

what do high levels of ketones cause and give examples

A

high levels of ketone bodies acetoacetate & beta hydroxybutyrate in blood affect pH, create ketoacidosis – this can be fatal – leads to coma and death

28
Q

why is cholesterol good and bad

A

needed as vital part of cell membrane
precursor to many molecules
high levels implicated in CVD and AD

29
Q

what are the two sources of cholesterol and give examples

A

from diet such as egg(yolk) liver, meat

synthesis in mainly liver and intestine

30
Q

what effect does plant sterols have on cholesterol uptake

A

inhibits uptake in the gut which helps lower plasma cholesterol

31
Q

describe cholesterol uptake from LDL via receptor mediated endocytosis

A

LDL binds to receptors on cell surface, LDL enters cells via cathrin coated pit and into vesicle then broken down by lysosome into cholesterol which is then repackaged

32
Q

what are the 4 steps of cholesterol biosynthesis

A

acetyl CoA to mevalonate (C6)
mevalonate to phosphorylated isoprene units (C5) - activation
polymerise 6 isoprene units to form c30 chain (squalene)
cyclisation to form ring structure (lanosterol) then cholesterol

33
Q

where does biosynthesis of cholesterol occur in the body

A

in cytosol and smooth endoplasmic reticulum

34
Q

how is synthesis of cholesterol controlled

A

by adjusting the activity or amount of HMG CoA reductase
high levels of cholesterol inhibit synthesis
insulin increases synthesis whereas glucagon inhibits

35
Q

how can you affect the enzyme of HMG CoA reductase to affect levels of cholesterol

A 
controlled of transcription of the enzyme (mRNA synthesis) 
- inhibited by high cholesterol 
- stimulated by insulin 
rate of degradation of enzyme
-increased by high cholesterol
36
Q

what is SREBP and what does it do

A

– sterol regulatory binding protein. When cholesterol levels in the ER membrane fall, it sets off a chain of reactions which cause the release of a protein SREBP from the membrance. This protein moves to the nucleus, binds to a sterol resonse elment on the DNA coding for certain genes, including HMG CoA reductase, and the LDL receptor ie stops more production of cholesterol

37
Q

how do humans get rid of cholesterol

A

cannot be broken down and only can be excreted in faeces via bile salts

38
Q

excess lipids are commonly associated with what diseases

A

coronary heart disease
strokes
alzheimers
steatohepatitis which leads to cirrhosis and hepatic carcinoma

39
Q

what is the uk target for cholesterol levels

A

5mM for healthy or less

4mM or less for those at risk

40
Q

what are the good vs the bad fats

A

mono/polyunsaturated fats are good

bad are saturated fats, trans fats and cholesterol

41
Q

what is the disease difference in high levels of HDL vs LDL

A

high saturated fats and cholesterol in diet causes increased risk of atherosclerosis and CHD
HDL involved in returning cholesterol from peripheral tissues to liver and decrease risk of atherosclerosis

42
Q

what is tangier disease

A

lack of HDL which increases risk of coronary disease

43
Q

what is atherosclerosis and how does it form

A

inflammatory response
damage to endothelial cells allows LDLs access to subintimal space
LDL become oxidised and are internalised by macrophages - foam cells
accusation of foam cells create bulge in vessel wall ie atherosclerotic plaque
fibrous collagen cap formed
plaque may restrict blood flow and cause angina in coronary vessels

44
Q

describe the link between cholesterol levels and alzheimer’s

A

Possession of the APOE4 allele (a form of lipoprotein involved in in cholesterol/lipid transport) increases the risk of developing Alzheimer’s disease

Most studies suggest that increased plasma cholesterol levels correlate with increased risk

High cholesterol diets in animal models cause accumulation of Aβ peptide (the main protein involved in plaques seen in diseased brain)

Some (but not all) studies report a link between statin therapy and decreased incidence of Alzheimer’s disease

45
Q

what does accumulation of fats in the liver lead to

A

inflammation and fibrosis which leads to hepatitis

46
Q

what is the difference between alcoholic and non-alcoholic steatohepatitits

A

AS - Metabolism of large amounts of alcohol disturbs the balance of fatty acid synthesis and oxidation, inhibiting fatty acid oxidation and activating excess triglyceride synthesis (caused by high NADH levels)

non-AS Insulin resistance leads to increased insulin secretion - this stimulates fatty acid synthesis

Body Systems (77 decks)

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