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Biochem I > Test 3 > Flashcards

Test 3 Flashcards

1
Q

what are lipids (4)

A

fats are lipids that are solid at room temp
oils are lipids that are liquid at room temp
Insoluble in water
Diverse functions: energy storage, structural, signaling

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2
Q

what are the classes of lipids (5)

A 
free fatty acids
triacylglycerols
phospholipids
glycolipids
steroids
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3
Q

what are storage lipids derived from

A

HIGHLY REDUCED hydrocarbon compounds called fatty acids

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4
Q

why are fatty acids called fatty “acids”

A

because one end contains a carboxylic acid

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5
Q

are most fatty acids even or odd numbered

A

even

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6
Q

what is the range in number of carbons

A

4 to 36

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7
Q

what are fatty acids with 0 double bonds called

A

saturated fats

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8
Q

what are fatty acids with 1 double bond called

A

monounsaturated fatty acid (MUFA)

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9
Q

what are fatty acids with 2 or more double bonds called

A

polyunsaturated fatty acid (PUFA)

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10
Q

How many kcal/g do lipids provide

A

9

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11
Q

how many kcals in ~1 pound of fat

A

3500

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12
Q

what is another name for fatty acids

A

acyls

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13
Q

what are the two areas of classification of fatty acids

A

number of carbons (length)

number of bonds (saturation)

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14
Q

How many carbons are present in a short chain fatty acid

A

4-6

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15
Q

how many carbons are present in a medium chain fatty acid

A

8-12

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16
Q

how many carbons are present in a long chain fatty acid

A

14-24

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17
Q

How many bonds are present in a saturated fatty acid

A

0

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18
Q

how many bonds are present in a MUFA

A

1

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19
Q

how many bonds are present in a PUFA

A

2 or more

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20
Q

Are saturated fatty acid oil or fat at room temp? and why?

A

fat. a lack of double bonds makes it easy for them to lay in uniform, tightly packed, crystalline formation

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21
Q

are MUFAs oil or fat at room temp and why

A

oil. the ‘kink’ created by the single double bond makes it difficult for the FA to lay down in uniform manner

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22
Q

are PUFAs oil or fat at room temp and why

A

oil. the multiple ‘kinks’ created by the multiple double bonds makes it difficult for the FA to lay down in uniform manner

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23
Q

What functional group is present at the omega end of all fatty acids (SFA, MUFAs and PUFAs)

A

methyl (CH3)

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24
Q

what functional group is found between double bonds in a PUFA

A

methylene (CH2)

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25
Q

what is the methylene group in PUFAs called

A

a methylene interrupter

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26
Q

what does the methylene group in PUFAs facilitate

A

rotation around the methylene group into several conformations

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27
Q

what are the two types of FA nomenclature

A

delta and omega

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28
Q

which end do you start counting from with delta nomenclature

A

the carboxylic acid group

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29
Q

which end do you start counting from with omega nomenclature

A

the methyl group end

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30
Q

what are some common patterns in FA (4)

A

even number of carbons
most common contain 12-24 carbons
most common bond is between c9 and c10 (delta)
double bonds are always 3 carbons apart

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31
Q

Name the Numbering, systematic name, and sources for PROPIONIC ACID

A

3:0, propanoic acid, fermented foods

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32
Q

Name the Numbering, systematic name, and sources for BUTYRIC ACID

A

4:0, butanoic, butter and goat milk

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33
Q

Name the Numbering, systematic name, and sources for CAPROIC ACID

A

6:0, hexanoic, goat milk

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34
Q

Name the Numbering, systematic name, and sources for CAPRYLIC ACID

A

8:0, octanoic, goat milk

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35
Q

Name the Numbering, systematic name, and sources for CAPRIC ACID

A

10:0, decanoic, goat milk

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36
Q

Name the Numbering, systematic name, and sources for LAURIC ACID

A

12:0, dodecanoic, coconut milk

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37
Q

Name the Numbering, systematic name, and sources for MYRISTIC ACID

A

14:0, tetradecanoic, coconut oil and palm oil

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38
Q

Name the Numbering, systematic name, and sources for PALMITIC ACID

A

16:0, hexadecanoic, palm oil, cocoa butter

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39
Q

Name the Numbering, systematic name, and sources for STEARIC ACID

A

18:0, octadecanoic, animal fats and cocoa butter

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40
Q

Name the Numbering, systematic name, and sources for ARACHIDIC ACID

A

20:0, eicosanoic, peanut oil, corn oil and cocoa butter

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41
Q

Name the Numbering, systematic name, and sources for LIGNOCERIC ACID

A

24:0, tetracosanoic, peanut oil

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42
Q

Name the Delta numbering, Omega numbering and sources for PALMITOLEIC ACID

A

16:1^9, 16:1w7, fish oil and macadamia nuts

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43
Q

Name the Delta numbering, Omega numbering and sources for OLEIC ACID

A

18:1^9, 18:1w9, olive oil and canola oil

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44
Q

Name the Delta numbering, Omega numbering and sources for NERVONIC ACID

A

24:1^15, 24:1w9, seed oils like flax

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45
Q

Name the Delta numbering, Omega numbering and sources for LINOLEIC ACID

A

18:2^9,12 , 18:2w6, corn, soy and sunflower oils

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46
Q

Name the Delta numbering, Omega numbering and sources for ALPHA-LINOLEIC ACID

A

18:3^9,12,15 , 18:3w3, flax, pumpkin, kiwi seeds, canola oils

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47
Q

Name the Delta numbering, Omega numbering and sources for ACARCHIDONIC ACID (ARA)

A

20:4^5,8,11,14 , 20:4w6, animal fats and eggs

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48
Q

Name the Delta numbering, Omega numbering and sources for EICOSAPENTANOIC ACID (EPA)

A

20:5^5,8,11,14,17 , 20:5w3, fish, algae and omega-3 eggs

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49
Q

Name the Delta numbering, Omega numbering and sources for DOCOSAHEXAENOIC ACID (DHA)

A

22:6^4,7,10,13,16,19 , 22:6w3, fish, algae, breast milk and omega-3 eggs

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50
Q

Are long chain lipids more or less soluble in water

A

less soluble

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51
Q

what does it mean to be more saturated

A

less double bonds

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52
Q

are short, medium and long chain fatty acids transported the same after absorption

A

no. short and medium are. long are different

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53
Q

what is the highest temperature an oil can be used at called

A

the smoke point

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54
Q

which oil has the highest smoke point

A

canola (468F)

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55
Q

Are there a lot of Free Fatty Acids found in the blood

A

no, very few

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56
Q

what do FFA bind to in blood and what kind of bond do they form

A

bind to albumin via noncovalent bonds

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57
Q

what type of specialized carriers transport long-chain fatty acids

A

chylomicrons

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58
Q

why can humans not synthesize omega-3 and omega-6 fatty acids

A

we lack enzymes called desaturases

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59
Q

which essential fatty acid do we consume the most of and what are 2 examples

A

18C variety, Linoleic acid (18:2w6) and alpha-linolenic acid (18:3w3)

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60
Q

what two steps are necessary to convert linoleic acid into arachidonic acid in the body

A

desaturation (adding double bonds) and elongation (adding carbons)

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61
Q

why is it important to get dietary DHA

A

because our body is extremely inefficient at converting from omega-3 to EPA to DHA

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62
Q

what is the more common name for triacylglyerols

A

triglycerides

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63
Q

how many carbons and fatty acids are attached to the glycerol backbone of a triglyceride

A

3 carbons

3 fatty acids

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64
Q

do most natural triglycerides contain the same fatty acid on all 3 locations

A

no

usually mixed and contain different fatty acids

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65
Q

what type of reaction creates triglycerides

A

dehydration

OH group from backbone and H from free fatty acids form 3 H20 molecules

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66
Q

what are triglycerides mainly stored for

A

energy

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67
Q

in what form are triglycerides stored in all cell

A

lipid droplets

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68
Q

why do muscles contain intramuscular triglyceride pools

A

for endurance exercises

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69
Q

What is the name of the special storage cells that store large amounts of triglycerides

A

adipocytes

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70
Q

why are TG better for energy storage than carbs (2)

A

carbon atoms in FA are more reduced than sugars, so oxidation of FA yields more than 2x as much energy per gram (9kcal/g vs 4kcal/g)

since TG are hydrophobic, fat storage doesn’t carry extra weight of water (2g H20/1g carb)

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71
Q

do we store more carbs or TG (in adipocytes)

A

less than a days worth of carbs

months worth of energy in adipocytes as TG (~80,000)

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72
Q

why do MUFAs and PUFAs go rancid more easily than saturated fats and triglycerides

A

oxygen attacks double bonds

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73
Q

what causes rancid aroma

A

oxidative breakage of double bonds yields aldehydes and carboxylic acids with shorter carbon chains

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74
Q

what is the difference between cis and trans fatty acids

A

cis FA can rotate around its double bonds

trans FA are stuck in a linear position

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75
Q

what does the fixed nature of trans FA cause it to behave like in the body

A

saturated fat (lays down in sheets, crystalline)

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76
Q

what catalysts is used to hydrogenate FA to make them trans

A

nickel and H2 gas

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77
Q

does trans fat increase of decrease risk of heart disease

A

increase

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78
Q

does trans fat increase of decrease LDL

A

increase

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79
Q

does trans fat increase of decrease HDL

A

decrease

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80
Q

are storage lipids neutral or polar

A

Neutral (glycerol backbone with 3 FA)

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81
Q

are membrane lipids neutral or polar

A

polar

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82
Q

which group of membrane lipids contain phosphate group

A

phospholipids

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83
Q

what are the two types of phospholipids

A

glycerophospholipids

sphingophospholipids

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84
Q

which group of membrane lipids contain carbohydrates

A

glycolipids

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85
Q

what is the only type of glycolipid

A

sphingolipids

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86
Q

what is the parent compound of glycerophospholipids

A

phosphatidic acid

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87
Q

what is each glycerophospholipid named for

A

the unique polar head group connected to the phosphate group

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88
Q

what are the 5 polar head groups that attach to glycerophospholipids

A

choline, serine, ethanolamine, glycerol, inositol

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89
Q

what is the most common phospholipid in the body and were is it especially concentrated

A

phosphatidyl-choline (lecithin)

concentrated in lung surfactant

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90
Q

what is phosphatidyl-serine a marker for

A

apoptosis

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91
Q

where is phosphatidyl-ethanolamine highly concentrated

A

brain and liver

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92
Q

what is phosphatidyl-glycerol a precursor for

A

cardiolipin

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93
Q

what is the major function of phosphatidyl-inositol

A

membrane anchoring and cell signaling

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94
Q

where is phosphatidyl-serine normally found

A

on the inner leaflet of the plasma membrane

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95
Q

what happens when phosphatidyl-serine moves to outer leaflet of plasma membrane

A

signals white blood cell to induce apoptosis

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96
Q

where is cardiolipin (diphosphatidyl-glyerol) exclusively found

A

on the inner mitochondrial membrane

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97
Q

describe the phospholipase C pathway

A

1) hormone binds to receptor starting cascade that activates phospholipase C
2) phospholipase C digest the inositol head group from phosphatidyl-inositol leave a diglyceride
3) The inositol release sequestered calcium from the endoplasmic reticulum.
4) The calcium plus the diglyceride activates protein kinase C which is a phosphorylating enzyme

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98
Q

what is an ether phospholipid

A

a phospholipid in which the 2 fatty acids are attached to the glycerol backbone with ETHER bonds rather than the typical ESTER bond

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99
Q

what are the two main ether phospholipids in the body

A

plasmalogen and platelet activating factor

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100
Q

what polar head group is required for the ether glycerophospholipid PLASMALOGEN

A

ethanolamine

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101
Q

what polar head group is required for the ether gylcerophospholipid PLATELET ACTIVATING FACTOR (PAF)

A

choline

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102
Q

which stereospecific number is the ether bond typically located at in plasmalogen

A

sn-1

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103
Q

where is most of the plasmalogen in the body found

A

50% is found in the brain

also found in heart, nerve and muscle

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104
Q

is the FA on SN1 of a phospholipid usually saturated on unsaturated

A

saturated

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105
Q

is the FA on SN2 of a phospholipid usually saturated or unsaturated

A

unsaturated

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106
Q

on which SN would you be most likely to find EPA in a phospholipid

A

SN2
typically where you find unsaturated FA
EPA is a MUFA

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107
Q

what type of backbone to sphingophospholipids contain

A

a sphingosine backbone

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108
Q

do sphingophospholipids contain a glycerol

A

NO

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109
Q

what is the parent compound of all sphinolipids

A

ceramide

110
Q

what two components make up a ceramide

A

sphingosine backbone plus a fatty acid

111
Q

what % of lipids in the stratum corneum are sphingophospholipids and what is their major function

A

50%-regulate water permeability of skin

112
Q

what four components are present in the sphingolipid sphingomyelin

A

sphingosine backbone + FA + Phosphate group + choline

113
Q

is sphingomyelin a phospholipid

A

yes - it contains a phosphate group

114
Q

what makes cerebrosides, globosides, and gangliosides different sphingomyelin

A

they don’t contain a phosphate group. They are sphingolipids but not sphingophospholipids

115
Q

what differentiates cerebrosides, globosides, and gangliosides from each other

A

the number of sugars attached

116
Q

what are the two types of sugar found on cerebrosides

A

glucose (found in non-neural tissue

galactose (found in neural tissue)

117
Q

what types of sugars are found on globosides

A

glucose, galactose, and N-acetylgalactosamine

118
Q

what is the feature that makes gangliosides unique from the cerebrosides and globosides

A

they always contain 3 or more sugars and must have N-acetylneuraminic acid attached

119
Q

how many sugars are found on globosides

A

2-4

120
Q

how many sugars are found on cerebrosides

A

1

121
Q

where are sphingolipids typically found in a plasma membrane

A

outer leaf

122
Q

what major hemolytic factor is determined by sphingolipids

A

blood type

123
Q

where does phospholipid degradation occur

A

in the lysosome

124
Q

what detrimental activity of sphingolipids may be caused by genetic defects

A

accumulation

125
Q

how many phospholipases are available to degrade sphingolipids. what are their names

A

4- A1, A2, C, D

126
Q

what does phospholipase C cleave from the glycerophospholipid

A

phosphate group and polar head group

127
Q

what does phospholipase D cleave from the glycerophospholipid

A

just the polar head group

128
Q

where does phospholipase A1 cleave

A

sn-1

129
Q

where does phospholiapase A2 cleave

A

sn-2

130
Q

what genetic disorder is exhibited as mental retardation due to a deficiency in sphingomyelinase (causing a an accumulation of sphingomyelin)

A

Neimann-Pick

131
Q

which two disorders are caused by an accumulation of gangliosides and what are the common symptoms

A

tay-sachs
sandhoff’s

blindness, muscle weakness

132
Q

what are the two disorders caused by accumulation of cerebrosides and what is the major symptom

A

gaucher’s
krabbe

CNS impairment

133
Q

which sugar is associated with gaucher’s

A

glucose

134
Q

which sugar is associated with krabbe

A

galactose

135
Q

what disorder is caused by an accumulation of ceramides and what is the major symptom

A

farber

joint deformity

136
Q

what disorder is caused by an accumulation of sphingomyelin and what is the major symptom

A

Niemann-Pick

neurodegeneration

137
Q

what is the most commonly known sterol

A

cholesterol

138
Q

what is the classification of cholesterol

A

steroid alcohol

139
Q

where is cholesterol made

A

in animal tissues

140
Q

where specifically is it synthesized

A

in the liver, small intestine and specialized tissue

141
Q

which organ regulates cholesterol

A

liver

142
Q

what are the major sources of liver cholesterol (3)

A

dietary cholesterol (chylomicron remnants)

endogenous cholesterol from extrahepatic tissues (HDL)

De novo synthesis in the liver from carbs, lipids and proteins

143
Q

when intake and synthesis are combined, how much cholesterol do we make per day

A

~1 gram

144
Q

what are three major outcomes for cholesterol (3)

A

secretion of VLDL

free cholesterol secreted in bile

conversion to bile acids/salts

145
Q

what coenzyme is required for endogenous cholesterol synthesis in the liver and intestines

A

Acetyl CoA

146
Q

what is the name of the rate limiting enzyme in cholesterol synthesis

A

HMG CoA reductase

147
Q

what is cholesterol required for

A

cell membrane integrity

148
Q

what is cholesterol a precursor for (3)

A

steroid hormones

bile

vitamin D

149
Q

which component of cholesterol faces the same direction as the polar head group on membrane lipids

A

hydroxyl group

150
Q

what are the two divisions of steroid hormones

A

sex hormones and corticosteroids

151
Q

what are the 3 classes of sex hormones

A

androgens (ie testosterone)

estrogens (ie estradiol)

progestagens (progesterone)

152
Q

what are the two classes of corticosteroids

A

glucocorticoids

mineralcorticoids

153
Q

what type of enzyme converts cholesterol to bile acids

A

cytochrome P450

154
Q

what % of bile is efficiently reabsorbed in the ileum

A

95%

155
Q

what happens to the 5% that is not reabsorbed

A

it is excreted in the feces

156
Q

how many grams of bile salt to we secrete daily

A

15-30 grams

157
Q

how much is lost in feces daily

A

~0.5 grams

158
Q

how much bile is made daily

A

~0.5 grams

159
Q

what vitamin that requires UVB radiation is a product of 7-dehydrocholesterol

A

vitamin D

160
Q

why can plant sterols be used as a treatment for hypercholesterolemia

A

they compete with cholesterol for absorption

161
Q

what are the three main functions of lipids (3 S’s)

A

Storage (80% of adipose)

Structure (5-10% of cell mass)

signaling

162
Q

what are the four major signaling abilities of lipids

A

hormones - travel in blood to another tissue

intracellular messaging

cofactors for enzymes

pigments for light absorption (IN PLANTS ONLY)

163
Q

what must happen to cholesterol to make it a steroid hormone

A

it must be oxidized

164
Q

what action of steroid hormones makes them a hormone

A

they travel through blood to other tissues

165
Q

why can steroid hormones exert an effect at very low doses

A

they have an extremely high affinity (low Km) for binding receptors

166
Q

once they reach the nucleus what effect do steroid hormones cause

A

changes in gene expression

167
Q

what makes steroid drugs (like prednisone) anti-inflammatory

A

they prevent the release of arachidonic acid from the plasma membrane

168
Q

what are the three major intracellular lipid signals

A

phosphatidyl-inositols

ceramide derivatives

eicosanoids

169
Q

what pathway is phosphatidyl-inositol 4,5-bisphosphate a part of

A

protein kinase c

170
Q

what is the major function of ceramide derivatives in intracellular signaling

A

REGULATION of a shitload of activities

171
Q

do eicosanoids travel in the blood

A

no- they are paracrine hormones that act only on adjacent cells

172
Q

what is an eicosanoid

A

a 20 carbon hormone-like compound

173
Q

what are the two divisions of eicosanoids

A

inflammatory and resolution

174
Q

what are the three subclasses of inflammatory eicosanoids

A

prostaglandins (PG)
Thromboxanes (TX)
Leukotrienes (LT)

175
Q

what are the two subclasses of resolution eicosanoids

A

Resolvins (Rv)

Lipoxins (LX)

176
Q

What are the 3 parts of eicosanoid naming

A

2 letter abbreviation (PG, TX)

3rd letter is order of discovery

subtext number tells us the number of double bonds (2=2, 3=3)

177
Q

what organ were prostaglandins first discovered in

A

prostate gland

178
Q

what are thromboxanes produced by

A

platelets called thrombocytes

179
Q

what do thromboxanes stimulate (2)

A

clot formation (platelet aggregation)

restriction of blood flow to clot site

180
Q

what type of drug inhibits thromboxane synthesis

A

NSAID

181
Q

what produces leukotrienes

A

white blood cells (leukocytes)

182
Q

what event, caused in part by leukotrienes, causes very strong smooth muscle contractions

A

anaphylactic shock

183
Q

what action does cyclooxygenase (COX) have on eicosanoids

A

removes 2 double bonds

184
Q

what action does lipoxygenase (LOX) have on eiconsanoids

A

scramble the order and location of the double bonds. Does not change the number of double bonds.

185
Q

what are the products of arachidonic acid after it goes through the COX pathway

A

2 series prostaglandins and thromboxanes (inflammatory, clotters)

186
Q

what is the product of arachidonic acid after it goes through the LOX pathway

A

4 series leukotrienes (inflammatory)

187
Q

what is the product of EPA after it goes through the COX pathway

A

3 series prostaglandins and thromboxanes (little to no effect)

188
Q

what is the product of EPA after it goes through the LOX pathway

A

5 series leukotrienes (little to no effect)

189
Q

will any given cell produce all the eicosanoids

A

NO - very selective

190
Q

which pathway does arachidonic acid prefer and why

A

COX

the COX way has a lower Km for ARA

191
Q

which pathway does EPA prefer and why

A

LOX

the LOX pathways has a lower Km for EPA

192
Q

how many isoforms of cyclooxygenase do mammals have

A

2

COX-1 and COX-2

193
Q

what is the function of COX-1

A

synthesize PG that regulate GASTRIC SECRETIONS

194
Q

what is the function of COX-2

A

synthesize PG that mediate inflammation, pain and fever

195
Q

which drugs are inhibitors for both COX 1&2

A

aspirin and ibuprofen

196
Q

what are the side effects of aspirin and ibuprofen

A

gastric irritation

197
Q

what are some selective COX-2 inhibitors

A

Celebrex, Vioxx

198
Q

what is the function of lipoxins and resolvins

A

combat the inflammation caused by the immune response (inflammation caused by fighting pathogens and also at the site of injury)

199
Q

what are lipoxins and resolvins collectively considered

A

protectins

200
Q

which two fatty acids are essential for the production of protectins

A

EPA and DHA

201
Q

what are the products of DHA after it has gone through the LOX pathway

A

D series resolving and D series protectin (both anti-inflammatory)

202
Q

which is more important in regard to cardiovascular disease risk. omega-6 to omega-3 ratio or saturated to unsaturated fatty acid ration

A

saturated to unsaturated fatty ratio

203
Q

what 4 types of fishes should be avoided in order to prevent mercury accumulation

A

shark
swordfish
tilefish from the gulf of mexico
king mackerel

204
Q

which dangerous cation of mercury is found in seafood

A

methyl mercury

205
Q

what antioxidant is decreased by an accumulation of methyl mercury

A

glutathione

206
Q

which omega-3 fatty acid prevents a decrease in glutathione

A

DHA

207
Q

what are the 4 fat-soluble vitamins

A

A, D, E, K

208
Q

Which two vitamins are precursors for hormones

A

A and D

209
Q

what is vitamin A called

A

retinol

210
Q

what organ is retinol vital to

A

eyes

211
Q

what is the name of active Vitamin D in the kidneys

A

calcitriol

212
Q

what is the major function of vitamins E and K

A

to act as coenzymes for redox reactions

213
Q

what part of the cell is vitamin an important antioxidant for

A

plasma membrane

214
Q

what is the typical intake of lipids each day

A

120-150 grams

215
Q

what % of lipids are absorbed

A

95-100%

216
Q

Is there digestion of triglycerides in the mouth and stomach

A

minimal

217
Q

what organ is essential for removing long chain FA from triglycerides

A

pancrease

218
Q

what is the primary function of bile released from the gallbladder

A

act as an emulsifier

219
Q

where are phospholipids and cholesterol digested

A

small intestine

220
Q

what is released in the mouth to start lipid digestion

A

lingual lipase

221
Q

what are the products of lingual lipase digestion and why

A

diglyceride and FA

it removes the FA from sn-3 on the triglyceride

222
Q

are lipids polar or nonpolar

A

nonpolar

223
Q

what activity must take place in order for lipids to be digested in the stomach

A

emulsification

224
Q

what is released from the pancreas in response to CCK

A

digestive enzymes

225
Q

what is released from the gallbladder in response to CCK

A

bile

226
Q

what is released from the pancreas in response to secretin

A

converts ATP to cyclic AMP.[19] Cyclic AMP acts as second messenger in intracellular signal transduction and causes the organ to secrete a bicarbonate-rich fluid that flows into the intestine.

227
Q

where are bile acids made

A

liver

228
Q

where are bile acids stored

A

gallbladder

229
Q

what are bile acids made from

A

cholesterol

230
Q

lipases from which organ digest 80% of triglycerides

A

pancreas (pancreatic lipases)

231
Q

what are the products of pancreatic lipase digestion

A

monoglyceride and 2 fatty acids

232
Q

what are the products of phospholipase A2 digestion

A

fatty acid and lysophospholipid

233
Q

what are the products of esterase digestion

A

fatty acid and free compounds (cholesterol, vitamin A and vitamin E

234
Q

Do brushborder lipases exist

A

NO

235
Q

what is formed when lipids coalesce with bile acids

A

micelles

236
Q

what type of lipid digestion occurs in the large intestine

A

trick question - none

and no fermentation of lipids either

237
Q

what form must lipids take in order to be absorbed

A

micelles

238
Q

what constitutes a micelle (5)

A

fatty acids
monoglycerides, fat-soluble vitamins
cholesterol
bile salts

239
Q

by what method are micelles absorbed

A

passive diffusion

240
Q

what parts of the small intestine are micelles absorbed in

A

the duodenum and jejunum

241
Q

by what process are the parts of the micelle turned into triglycerides, phospholipids and cholesterol esters in the smooth endoplasmic reticulum of enterocytes

A

reesterfication

242
Q

what are micelles packaged into in Golgi complex

A

chylomicrons

243
Q

what types of fatty acids are the exception to the rule and how do they get to the liver

A

short and medium chains pass directly into the portal vein

244
Q

what are causes of lipid malabsorption (3)

A

impaired digestion or absorption

cystic fibrosis

bile acid insufficiency

245
Q

what are the signs of lipid malabsorption

A

STEATORRHEA (fatty stools)

246
Q

how do you treat lipid malabsorption (2)

A

limit fat intake

supplement with pancreatic lipase and/or bile salt

247
Q

what is the name of the special lipid carrier and why is it necessary

A

lipoprotein

because lipids are hydrophobic

248
Q

what are the three parts of a lipoprotein

A

phospholipid exterior
lipid core
apoprotein

249
Q

what is the function of the apoprotein

A

it is the protein portion and binds to receptors

250
Q

what are examples of lipoproteins

A

chylomicrons
VLDL
LDL
HDL

251
Q

what are dietary fats and fat-soluble vitamins transported by

A

chylomicrons

252
Q

what is the most prevalent component of chylomicrons

A

triglycerides

253
Q

which system do chylomicrons travel through and what is their final destination

A

through the lymphatic system and eventually to adipocytes

254
Q

which type of cells express lipoprotein lipase

A

endothelial cells

255
Q

what activates lipoprotein lipase

A

apoprotein on chylomicrons and VLDL

256
Q

what is the function of lipoprotein lipase

A

break down triglycerides into glycerol and fatty acid

257
Q

how long does a chylomicron stay in circulation

A

~14 hours

258
Q

where is a chylomicron recycled to after it is depleted of triglycerides

A

the liver

259
Q

what transport molecules carry fat that ends up in the liver

A

VLDL

260
Q

what do VLDLs have more of then chylomicrons

A

cholesterol

261
Q

what does VLDL deliver to cells

A

triglycerides

262
Q

after depleting its triglyceride stores what does a VLDL become

A

a cholesterol rich LDL

263
Q

what genetic variation causes familial hypercholesterolemia

A

lack of LDL receptors

264
Q

what happens to LDL (the cholesterol rich remnants of VLDL)

A

It is internalized by endothelial cells via receptor-mediated endocytosis

265
Q

what form of cholesterol can HDL pick up

A

free cholesterol (OH group, no ester bond and additional fatty acid)

266
Q

what form of cholesterol can HDL not pick up

A

cholesterol ester

267
Q

by what means does free cholesterol regulate cellular cholesterol concentrations (3)

A

with inhibiting rate-limiting enzyme (HMG CoA reductase)

by decreasing the synthesis of LDL receptors

by promoting cholesterol storage as cholesterol ester

268
Q

after HDL picks up free cholesterol from cells where does it take it and what happens to it

A

back to the liver and converted to bile salt

269
Q

which fatty acids increase LDL

A

lauric
myristic
palmitic
any trans fats

270
Q

which fatty acids have no effect on LDL

A

stearic acid

271
Q

which fatty acids decrease LDL

A

MUFA

PUFA

Biochem I (1 decks)

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