FATTies (lipids) Flashcards

1
Q

3 primary functions of lipids

A
  • energy
  • essential FAs for FA synthesis
  • absorption of essential fat-soluble vitamins
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2
Q

3 non-primary functions of lipids

A
  • precursor for steroid hormones
  • structural component of cell membranes
  • signaling molecule and electrical insulators
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3
Q

AMDR of lipids

A

20-35% of daily energy intake (greater than 35% not recommended)

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4
Q

how much of your total energy consumption should be from saturated fat?

A

less than 10%

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5
Q

how do lipids travel through the bloodstream, given that they are hydrophobic?

A

they attach to binding proteins like albumin or lipoproteins

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6
Q

3 classes of lipids

A

triglycerides
sterols
phospholipids

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7
Q

triglycerides

A
  • aka triacylglycerol
  • primarily a source of energy
  • composed of 3 fatty acids and a glycerol (bonded by esterification)
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8
Q

esterification

A
  • the bonding of fatty acids to glycerol to make triglycerides
  • occurs in liver, enterocytes and adipocytes
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9
Q

fatty acid lengths and number of Cs

A
  • short chain: less than 6
  • medium chain: 6-12
  • long chain: greater than or equal to 14
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10
Q

ways to categorize fatty acids

A

short, medium, or long
saturated or unsaturated
trans or cis

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11
Q

what is saturated (re fatty acids)?

A

all carbons in the fatty acid chain are saturated with hydrogens: no double bonds between Cs

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12
Q

what is unsaturated (re FAs)?

A

one or more double bonds between Cs: monounsaturated (1 db) or polyunsaturated (2+ db)

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13
Q

how are polyunsaturated acids classified?

A

omega-3 and omega-6: based on position of first double bond after the omega carbon.

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14
Q

alpha-linolenic acid (ALA): omega 3 or 6? essential or nonessential? inflammatory or anti-inflammatory?

A

omega 3. essential. anti-inflammatory effect.

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15
Q

linoleic acid (LA): omega 3 or 6? essential or nonessential? inflammatory or anti-inflammatory?

A

omega 6. essential. inflammatory in excess.

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16
Q

why is ALA important/distinct?

A

it is a precursor to other fatty acids, like DHA and EPA

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17
Q

how are synthetic trans fatty acids created and why?

A
  • by adding H to liquid vegetable oils (MUFA or PUFA)

- to make them more solid, to better texture and taste, for frying, and to increase shelf life

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18
Q

how are trans fatty acids listed on labels?

A
  • hydrogenated or partially hydrogenated

- if less than 0.5g, they can say “0 trans fats”

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19
Q

why are trans fats bad?

A

they raise LDL and lower HDL

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20
Q

what class of dietary fat is cholesterol?

A

sterol

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21
Q

is cholesterol essential or nonessential?

A

nonessential: synthesized in the liver

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22
Q

what are dietary sources of cholesterol?

A

animal products like eggs

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23
Q

functions of cholesterol

A
  • component of all cell membranes
  • needed for production of testosterone, estrogen, adrenal hormones, and vit D
  • needed for production of bile (to digest fats)
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24
Q

phospholipids: essential or no?

A

nonessential nutrient

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25
Q

what are dietary sources of phospholipids?

A

most plants and animals contain them in their cell membranes.

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26
Q

functions of phospholipids

A
  • cell membranes (phospholipid bilayer)
  • supply fatty acids for cellular metabolism
  • incorporated into the outer surface of lipoproteins (lipid transporters)
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27
Q

what class of dietary fat is lecithin?

A

phospholipid

28
Q

3 enzymes (i think?) used to break down lipids

A
  • lingual lipase
  • pancreatic lipase
  • bile from gallbladder
29
Q

what are triglycerides broken down to by lipase and bile? what form do these products take?

A

monoglycerides and free fatty acids. they form micelles.

30
Q

what would happen if a person didn’t make bile?

A

lipid absorption would drop from 97% to 50%

31
Q

how are monoglycerides and fatty acids absorbed into the enterocytes?

A

via passive diffusion

32
Q

what happens to MGs and FAs once they enter the enterocytes?

A

they are esterified back into triglycerides in the endoplasmic reticulum of the enterocytes. then they are combined with cholesterol, apolipoprotein, and phospholipid to form a chylomicron (a type of lipoprotein)

33
Q

chylomicron

A
  • a lipoprotein made of TG, cholesterol, apolipoprotein, and phospholipid
  • formed in the enterocyte
  • allows for the transport of dietary TGs in aqueous environment of the blood and lymph (phospholipid heads and proteins are hydrophilic)
  • short-lived: metabolized a few hours after a meal
34
Q

lipoprotein vs apolipoprotein

A

lipoprotein is a particle; apolipoprotein is a protein (part of lipoprotein particle)

35
Q

where does a chylomicron go once it’s formed in the enterocyte?

A

they leave the enterocyte, enter the lymphatic system, and then drain into the venous system via the subclavian vein (takes 3 hours)

36
Q

where do chylomicrons change from lymph to blood?

A

the subclavian vein

37
Q

what types of fatty acids are not included in the chylomicron, and how do they enter the bloodstream?

A

SCFAs and MCFAs, and they enter the blood directly from enterocytes (kinda like monosaccharides)

38
Q

while chylomicrons are floating around the bloodstream, who do they need to bump into to get absorbed into cells?

A

lipoprotein lipase (LPL)

39
Q

what is lipoprotein lipase? where is LPL located? what does it do?

A

it is an enzyme found in the capillaries of adipose, muscle and liver tissues. LPL stimulates lipolysis, which breaks down TG into glycerol and FAs, which can then enter these cells

40
Q

lipolysis

A

the breakdown of TG into FA and glycerol, which can then enter muscle and adipose cells.

41
Q

what happens to FAs in muscle cells?

A

they can be used as a source of energy, or they can combine with glycerol (esterification) to form intramuscular triglycerides (IMTG)

42
Q

what happens to FAs in adipose cells?

A

they combine with glycerol to form TGs (esterification)

43
Q

in what form are fatty acids sent to the liver from enterocytes/the bloodstream?

A

chylomicron

44
Q

4 types of lipoproteins

A
  • chylomicrons
  • LDL
  • HDL
  • VLDL
45
Q

VLDL

A
  • very low density lipoproteins
  • synthesized in the liver
  • transports endogenous fats (as opposed to dietary fats): mostly TG made in the liver from excess glucose
  • once TG are released, VLDL are converted to LDL
46
Q

LDL

A
  • low-density lipoproteins
  • synthesized in the liver
  • transports cholesterol
  • high levels of LDL increase risk of CVD, because if there’s too much LDL, it will deposit cholesterol into the blood vessel walls
  • “bad” cholesterol
47
Q

HDL

A
  • high-density lipoproteins
  • synthesized in the liver
  • removes cholesterol, decreases risk of CVD
  • “good” cholesterol
48
Q

what is the leading cause of death globally (32% of all deaths)? (1 in 4 deaths)

A

heart disease (aka cardiovascular disease)

49
Q

what conditions count as CVD?

A
  • blood vessel disease (ie coronary artery disease)
  • arrhythmias
  • congenital heart defects
  • heart valve disease
  • heart infections
50
Q

coronary artery disease

A

atherosclerosis (plaque build up in arteries) in the arteries that carry blood to the heart

51
Q

pectoris angina

A

chest pain (from restricted blood flow because of atherosclerosis)

52
Q

thrombosis

A

blood clot from when plaque ruptures and clotting is needed to stop the internal bleeding. stationary in the artery walls.

53
Q

embolus

A

a thrombosis that dislodges from the blood vessel and is carried in the blood (depending on where it lands it can cause a heart attack or stroke)

54
Q

myocardial infarction

A

heart attack

55
Q

what are the 4 main coronary arteries?

A
  • right coronary artery
  • left coronary artery
  • left anterior descending artery
  • left circumflex artery
56
Q

what are the 3 layers of the artery wall?

A
  • intima (inside)
  • media (middle)
  • adventitia (outside)
57
Q

occlusion

A

when a thrombosis (blood clot) completely blocks the artery

58
Q

between which layers of the artery does a fatty streak/plaque develop?

A

the intima and media

59
Q

dyslipidemia

A

abnormal blood lipid levels:

  • low HDL
  • high LDL (most important)
  • high total cholesterol
  • high TG
60
Q

what type of medication lowers LDL? what are other lifestyle ways to lower it?

A

statins. aerobic exercise and diet modification.

61
Q

how does aerobic exercise help with lipid levels?

A
  • lowers LDL
  • lowers TG
  • raises HDL
62
Q

what are dietary modifications to improve lipid levels?

A
  • fiber-rich diet
  • reduce saturated fat intake
  • avoid trans fats
  • fatty fish/fish oil
  • moderate alcohol consumption
  • replace full fat dairy with low fat
63
Q

what does saturated fat do to lipid levels?

A

it raises LDL (specifically pattern A type, which is not linked to coronary heart disease), but it also raises HDL

64
Q

does pattern A or B LDL increase risk factor for CVD?

A

pattern B LDL

65
Q

foods high in monounsaturated fats

A
  • nuts and seeds
  • olive oil
  • canola oil
  • avocado
  • peanut oil
  • sesame oil
  • high oleic oils
66
Q

what are the 3 types of omega-3 FAs? health benefits of omega-3 PUFAs

A

ALA (plant sources), DHA and EPA (fish sources): essential fatty acids

  • all 3 are cardioprotective: DHA and EPA are most potent
  • lower TGs
  • increase HDL
  • prevents blood clotting
  • lowers blood pressure
  • decreases arrhythmia
  • anti-inflammatory