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PATH30003- Frontiers in Human Disease > Lecture 11- Lipid metabolism > Flashcards

Lecture 11- Lipid metabolism Flashcards

1
Q

fatty acids

A

most energy rich molecule, possible endocrine function

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2
Q

triglycerides

A

transport and storage vehicle for FA’s from place to another

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3
Q

phospholipids

A

structural basis of membranes, intracellular signalling

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4
Q

sterols

A

regulation of membrane fluidity, some play endocrine function (hormones)

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5
Q

cholesteryl esters

A

transport and storage vehicle for cholesterol

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6
Q

prostaglandins

A

intracellular signalling, endocrine function

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7
Q

vitamins

A

cofactors for different enzymes

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8
Q

how do lipids move?

A

they are insoluble in water

- bound by an apolipoprotein to form a lipoprotein complex in order to move inside or in between cells in a complex

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9
Q

lipoprotein complex

A

lipid and apolipoprotein

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10
Q

LDL

A

low density cholesterol- bad

- moves cholesterol into cell

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11
Q

HDL

A

high density cholesterol- good

- moves cholesterol out of cell

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12
Q

process of lipid metabolism

A

lipids from diet–>intestine absorbs lipids, TG’s, cholesterol and packages in chylomicrons–>TG’s can be hydrolysed, release FA’s–>liver takes up some where they catabolise and release VLDL gradually–>VLDL release FA’s becomes LDL (less TG’s but lots of cholesterol)–>cholesterol taken up by cells, most goes back to liver through reverse cholesterol transport–>impaired then cholesterol accumulates in plasma

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13
Q

chylomicrons

A

lipoprotein particles consisting of TGs, phospholipids, cholesterol, proteins
-rich in energy

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14
Q

reverse cholesterol transport

A

HDL takes excess cholesterol back from peripheral cells via ABCA1 transporter

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15
Q

hypercholesterolemia

A

cholesterol accumulates in plasma

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16
Q

ABCA1 transporter

A

cholesterol efflux to HDL which takes cholesterol back to liver

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17
Q

tangier disease

A

impaired reverse cholesterol transport

  • mutation in ABCA1 transporter
  • increased risk of CHD, lipid deposits
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18
Q

mutation in ABCA1 transporter

A

tangier disease- impaired reverse cholesterol transport

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19
Q

atherosclerosis

A

accumulation of cholesterol in vessel wall of artery–>plaque grows, obstructs 95% of vessel to feel symptoms—>necrosis

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20
Q

rupturing of atherosclerotic plaque

A

ruptures–>become thrombogenic, form thrombin which can detach and travel to smaller vessels and block them–> they will get no oxygen and area dies

21
Q

elements of atherosclerosis

A

accumulation of macrophages into vessels wall, loading macrophages with cholesterol (cant get out)–>foam cells

  • modification of SMC, less contractile, synthesise ECM, accumulates
  • necrosis
22
Q

foam cells

A

hallmark of atherosclerosis

- macrophages fully filled with cholesterol esters in vesicles (difficult to get rid of)

23
Q

balancing act mechanisms

A
  • cell regulates own cholesterol level- reduces cholesterol biosynthesis and LDL uptake; but only so far
  • cholesterol efflux- removes cholesterol through reverse cholesterol transport
  • macrophages synthesise cholesterol esters in vesicles
24
Q

familial hypercholesterolemia

A

mutation of gene for LDL receptor- dominant trait

25
Q

consequences of familial hypercholesterolemia

A

LDL not cleared, stays in plasma, gets modified, elevated plasma LDL, abnormal cholesterol deposition

26
Q

heterozygous for LDL receptor mutation

A

1 in 200

- uptake of LDL by liver is slowed

27
Q

homozygous for LDL receptor mutation

A

1 in a million

-no LDL uptake, 100% fatal, multiple MI in childhood

28
Q

statins

A

act on level of liver, reduce amount of cholesterol in liver

  • competitive inhibitors of HMG CoA reductase (inhibits cholesterol biosynthesis)
  • liver thinks cells dont have enough cholesterol, upregulate LDL receptors in liver due to limited supply of endogenous cholesterol
  • decrease plasma LDL cholesterol levels up to 40%
  • reduces coronary events by 34%
29
Q

HMG CoA reductase

A

produces cholesterol

30
Q

PCSK9

A

binds to LDL-R, causes degradation of both PCSK9 and LDL-R inside endosome–>therefore less LDL-R at cell surface

31
Q

PCSK9 inhibitors

A

stop binding of PCSK9 to LDL-R

  • therefore LDL-R releases cholesterol inside endosome
  • LDL-R recycles back to surface, can uptake more LDL
  • decreases plasma LDL-C levels up to 70%
32
Q

North Karelia Project

A

incidence of death by heart disease higher than anywhere else

  • change diet, stop smoking, hypertension reduced
  • CVD mortality decreased by 73%
33
Q

Alzheimer’s disease and cholesterol

A

misfolding of proteins (Abeta and tau) occurs in lipid rafts

  • number of rafts in brain higher than anywhere else
  • abundance of rafts depends on cholesterol content
  • AD may be consequence of impairment of cholesterol metabolism in brain
34
Q

lipid rafts

A

part of plasma membrane that is rich in cholesterol and solid- proteins (Abeta, tau) that get there do not dissociate apart

35
Q

criteria for metabolic syndrome

A

waist circumference, elevated TG’s, low HDL-C, high blood pressure, serum glucose

36
Q

aetiology for obesity

A

increase in adipose tissue (rich in TGs)–>release FA’s–>effective energy source, so cell doesnt use glucose–>shut downs glucose transport–>glucose concentration in plasma goes up–>pancreas think that cells dont have enough insulin–>produces more insulin–>cells shut down insulin receptors–>hyperinsulinemia–>pancreatic Beta cells stress and damage–>hyperglycemia

37
Q

hyperinsulinemia

A

excess levels of insulin in blood compared to glucose

38
Q

hyperglycemia

A

excess glucose in bloodstream

39
Q

lifestyle treatment for low HDL

A

clinical outcomes are certain but not sure whether benefits are caused by raising HDL

40
Q

drug treatment for low HDL

A

increase HDL but clinical outcomes of treatment are uncertain

41
Q

CETP inhibitors

A

inhibits CETP (changes mature HDL into VLDL-LDL)

42
Q

CETP inhibitors consequences

A

increases HDL-C by 50-100%

  • thought it would reduce CVD by 40-50%
  • first CETP inhibitor completely ineffective,increased HDL-C but did not reduce CVD
  • how to make raising HDL a good thing?
43
Q

3 major ways we release energy

A 
basal metabolism (60-75%)
thermogenesis (10%)
physical activity (15-30%)
44
Q

evolutionary view of energy balance

A

issue of insufficient food- left to individual

excessive food- resolved on population level

45
Q

lipostatic model

A

restoration of weight to set point

46
Q

mechanism of energy balance

A

diet–>adipose tissue goes down (biggest producer of leptin- make you feel full)–>reduced leptin–>leptin receptor in brain signals not enough food so increase food uptake–>insulin receptors say reduce energy expenditure
- NPY/AgRP- stimulates appetite
Melanocortin- decrease appetite

47
Q

weight loss

A

reduction in core body temperature
reduced sympathetic tone
reduced thyroid function T3/4
perception of fullness, consumption, taste altered
20% increase in muscular efficiency, fat burning

48
Q

obesity paradox

A

people with high BMI survived longer

49
Q

possible reasons for obesity paradox

A

fitness vs fatness
BMI vs adiposity
action bias (what you do after you got sick)
treatment bias (obese patients receive treatment)
duration bias (studies were short term)
selection bias

PATH30003- Frontiers in Human Disease (20 decks)

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