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NUTR-455 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

length of short, medium, and long chain FA

A

6
6-10
>=12

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2
Q

majority of dietary FA are this length

A

long chain

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3
Q

Delta system of FA naming count carbons from this end

A

carboxyl end

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4
Q

omega system of FA naming count carbons from this end

A

methyl end

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5
Q

properties of SFA (2)

A

solid a room temp

single bonds

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6
Q

found in animal fats, palm oil, palm kernal oil, coconut oil

A

SFA

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7
Q

properties of MUFAs (2)

A

generally plant based

one double bond

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8
Q

examples of this FA are olive oil, peanut oil, canola oil

A

MUFA

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9
Q

Properties of PUFAs (2)

A

more than one double bond

generally plant based, but also found in fish

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10
Q

examples of this FA are corn oil, sunflower oil, fish oils, nuts and seeds

A

PUFAs

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11
Q

Properties of Trans fatty acids (5)

A 
Trans configuration double bond
form naturally, or thorugh hydrogenation of PUFA
extend shelf life
increase baking properties
solid at room temp
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12
Q

T/F: hydrogenated oils, or partialy hydrogenated vegetable oil on a label is the same as SFA

A

F, Trans fats

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13
Q

T?F: TFA are found in fried food, commercial baked goods, processed foods, and margerine

A

T

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14
Q

Linoleic acid (omega-6) and alpha-linolenic acid (omega 3) are examples of this

A

essential fatty acids

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15
Q

Reason why there are essential FA

A

your body cannot from CC double bonds before the 9th carbon, it does not have the correct enzymes

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16
Q

This is the enzyme in plants that can make the essential FA that animals are lacking

A

desaturase

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17
Q

This essential fatty acid deficiency disease causes growth retardation, skin disorders, infection susceptibility, and poor wound healing

A

cystic fibrosis

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18
Q

acid and alcohol coming together from this type of bond

A

ester bond

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19
Q

triglycerides are made of these compounds

A

glycerol and 3 FA bound by ester bonds

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20
Q

linoleic, y-linolenic, arachidonic acid are all examples of

A

omega 6 FA

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21
Q

a-linolenic, stearidonic, eicosapentaenoic, docosahexaenoic acids are all forms of

A

omega 3 FA

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22
Q

these make up 95% of dietary fat

A

TAG

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23
Q

enhanced taste and texture, energy, supply essential fatty acids, carriers of fat-soluble compounds, storage from of energy, and cell signaling/gene expression are all functions of this structure

A

TAG

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24
Q

Easiest way to remove cholesterol from the body is through this mech

A

GI tract

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25
Q

T/F: a cholesterol molecule is a steroid molecule with an extra OH, CH3, and FA group attached to it

A

t

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26
Q

What makes a cholesteryl ester different that a cholesterol molecule

A

cholesteryl ester have a FA bound to the OH group through an ester bond

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27
Q

Sex hormones, bile acids, vitamin D, and corticosteroids are made from these

A

sterols and steroids

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28
Q

What is helpful about ingestion of phytosterols

A

they help eliminate cholesterol through the diet (compete for absorption)

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29
Q

These function as emulsifiers, cell membrane and lipoprotein components

A

phospholipids

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30
Q

T/F: phospholipids can interact with polar and non polar compounds

A

T

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31
Q

In most cases the two FA tails on a phospholipid are this type of FA

A

SFA

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32
Q

The hydrophilic portion of a phospholipid is called this

A

polar head group

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33
Q

Phospholipids act as signaling molecules which lead to the activation of this, or the release of this

A

activation of protein kinase C leading to enzyme activation

release of Ca2+ leading to enzyme activation, or other hormonal responses

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34
Q

This is the main phospholipid

A

lecithin

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35
Q

these have a SFA in position 1 and a UFA in position two

A

glycerophosphatides

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36
Q

examples of a glycerophosphatide

A

lecithin, cardiolipin

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37
Q

a type of phospholipid that is abundant in nerve tissue

A

sphingolipids

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38
Q

This are structural lipids in nerves and brain tissue that have a saccaride component

A

glycolipids

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39
Q

Estimated intake of TAG, PL, Chol/phytosterols

A

100-150 g/d
~5 g/d
200-400 mg/d

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40
Q

Fat spoils due to this

A

oxidation

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41
Q

these accelerate oxidation of fat

A

double bonds

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42
Q

these factors limit fat oxidation (4)

A

limit exposure to air
cold temp
antioxidants
partial hydrogenation

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43
Q

This enzyme is used to convert eholesterol esters into cholesterol and FFA

A

Cholesterol esterase (cholesterol ester hydrolase)

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44
Q

How does bile aid in lipid digestion

A

increases surface area of the lipids, so enzymes can interact

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45
Q

How does lingual lipase aid in lipid digestion

A

it is good at cleaving short chain FA

Turns TAGs into DAGs and FFA

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46
Q

This enzyme accounts for 10-30% TAG digestion

A

gastric lipase

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47
Q

Gastric lipase aids lipid digestion by

A

it is good at cleaving short chain FA

Turns TAGs into DAGs and FFA

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48
Q

How does pancreatic lipase aid in lipid digestion

A

breaks down the ester bonds on the ends of the TAG to from MAGs and 2FFA

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49
Q

The majority of lipid digestion occurs here

A

upper jejunum

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50
Q

How does phospholipase A2 aid in lipid digestion

A

removes the middle FA from a phospholipid forming a FFA and a lysophospholipid

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51
Q

a lysophospholipid is this

A

a digested phospholipid

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52
Q

Cholesterol esterase is produced here, and acts on this

A

pancreatic acinar cells

sterol esters

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53
Q

These four compounds are produced by pancreatic acinar cells

A

cholesterol esterase
phospholipase A2
Procolipase
pancreatic lipase

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54
Q

gastric lipase is produced by this

A

chief cells of the stomach

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55
Q

how does colipase aid in lipid digestion

A

activates pancreatic lipase

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56
Q

Examples of pancreatic lipase inhibitors

A

orlistat
xenical
alli

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57
Q

why should people take a pancreatic lipase inhibitor

A

trouble with lipid digestion

weight loss

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58
Q

The 5 final products of lipid digestion

A 
lysophospholipids
nonesterified (free) cholesterol
nonesterified (free) FA
Nonesterified (free) Plant Sterols
2-Monoglycerides
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59
Q

This is a way to deliver FA and fat soluble vitamins in an aqueous enviornment

A

mixed micelles

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60
Q

This percent of FA are absorbed in the diet, and this percent of cholesterol

A

> 95%

~50%

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61
Q

This percent of FA in the diet are LCFA

A

92-96%

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62
Q

This carries medium chain fatty acids in the blood

A

albumin

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63
Q

How are SCFA and MCFA absorbed

A

directly into the capillaries

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64
Q

T/F: use medium chain FA if you have a hard time absorbing lipids such as in cystic fibrosis

A

T

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65
Q

This FA length increases energy expenditure after a meal

A

MCFA

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66
Q

The mixed micelle interacts with this

A

untirred water layer of the brush boarder

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67
Q

FFA go here, while the Chylomicron formed from the golgi app. go here

A

portal vein

lymphatic system

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68
Q

most important protein on a chylomicron

A

apo B-48

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69
Q

Chylomicrons from here

A

distal duodenum and jejunum

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70
Q

the majority of the chylomicron is made up of this

A

triglycerides

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71
Q

T/F: LCFA first go to the liver, while SCFA and MCFA first go to systemic circulation

A

F

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72
Q

Chylomicron activity peaks this long after a meal

A

30 min

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73
Q

the lymp system goes to tissues in this order

A

muscles
adipose
liver

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74
Q

this enzyme is in the adipose, muscle, mammary gland, brain, macrophages, and kupffer cells

A

lipoprotein lipase (LPL)

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75
Q

this enzyme facilitates deposition of FAs in tissues for storage or energy production

A

lipoprotein lipase (LPL)

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76
Q

In this state, activity is high in adipose and low in skeletal and heart muscle for LPL

A

fed state

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77
Q

In this state, activity is low in adipose and high in skeletal and heart muscle for LPL

A

fasted

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78
Q

These carry absorbed dietary lipids, carry lipids from liver to cells, and carry lipids to liver for excretion

A

lipoproteins

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79
Q

examples of lipoproteins (4)

A

chylomicron
VLDL
LDL
HDL

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80
Q

characteristic apoprotein for VLDL

A

apo B-100

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81
Q

characteristic apoprotein for LDL

A

apo B-100

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82
Q

characteristic apoprotein for HDL

A

apo A-I

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83
Q

These act as identification, stablizie, specificity, and aid in recognition of lipoproteins

A

apoproteins

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84
Q

chylomicrons originate here

A

golgi app of intestinal cells

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85
Q

chylomicrons are composed of

A

mostly TAG with little phospholipid, cholesterol and protein

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86
Q

VLDL originate here

A

liver (golgi app)

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87
Q

VLDL are composed of

A

mostly TAG with a little more phospholipids, cholesterol, and protein than chylomicrons

88
Q

carry lipids from liver to cells, deliver TG to cells then shrink to become IDL

A

VLDL

89
Q

LDL originate from this

A

IDL

90
Q

LDL are taken up by this

A

B-100 receptors fround in the liver and hon-hepatic tissue

91
Q

These are generated from the VLDL during circulation, carry lipids to cells, mainly carry cholesterol (large proportion), uptaken by LDL receptor

A

LDL

92
Q

Chylomicrons follow this pathway, while VLDL and IDL follow this pathway

A

exogenous

endogenous

93
Q

T/F: the more cholesterol in the cell, the less LDL receptors are formed

A

T

94
Q

This occurs when LDL is absorbed in the cell

A

lysosome digests

free cholesterol is packaged by the golgi app, and esterified with ACAT and stored in the cell

95
Q

exogenous lipids (gut to liver)

A

chylomicron

96
Q

endogenous lipids (liver to periphery)

A

VLDL

LDL

97
Q

reverse transport (periphery to liver)

A

HDL

98
Q

synthesized from liver and intestine in a lipid free nascent form

A

HDL

99
Q

Mostly protein composes its structure

A

HDL

100
Q

This LP returns lipids (cholesterol) to liver for re-use or excretion

A

HDL

101
Q

T/F: there are smaller fluctuations in LDL and HDL concentrations in the blood than in CM, VLDL, IDL

A

T

102
Q

This tissue synthesizes bile salts, VLDL, HDL, and new lipids from non-lipid precursors

A

Liver

103
Q

this tissue absorbs TAG and cholesterol from chylomicrons through lipoprotein lipase, and stores TAG

A

adipose tissue

104
Q

What is lipoprotein lipase

A

found on adipose and muscle tissue, removes FA from TAGS in chylomicrons and VLDL and brings them into the cell

105
Q

this helps to transfer cholesterol to the liver and eventually excrete it

A

cholesterol ester transfer protein

106
Q

This percent of adipose tissue is lipid material

A

85%

107
Q

HDL acts inconjuction with these two enzymes to move cholesterol from the peripheral tissues to the liver via the plasma

A

cholesterol esterifying enzyme

lecithin: cholesterol acyltransferase (LCAT)

108
Q

these are cholesterol delivery trucks, and increase risk of CVD

A

LDL

109
Q

these are cholesterol garbage trucks and perform reverse cholesterol transport, decrease risk of CVD

A

HDL

110
Q

Chylomicrons are made here

A

enterocytes

111
Q

secretion of chylomirons

A

exogenous, intestinal cell to lymph, to blood

112
Q

chylomicrons change to this during dirculation

A

chylomicron remnant

113
Q

physiological role of chylomicrons

A

deliver FA to the peripheral cells (adipocytes)

114
Q

Key enzyme in cholesterol synthesis

A

HMG-CoA reductase

115
Q

What is the rate-limiting step of cholesterol synthesis

A

HMG-CoA reductase

116
Q

where are VLDL and LDL synthesized

A

hepatocytes

117
Q

where is HDL synthesized

A

hepatocytes (80%) enterocytes (20%)

118
Q

earliest stage of HDL

A

nascent HDL

119
Q

First step of FA metabolism

A

extract lipids from LP via LPL (lipoprotein lipase)

120
Q

the cleavage of a staturated CC bond during FAox yields this many ATP

A

5

121
Q

Glycerol cannot be utilized by the cell, so it is sent here

A

liver

122
Q

Phase 1 of FA oxidation

A

activation of FA by CoA (acyl-CoA synthetase) forms Acyl-CoA

123
Q

Phase 2 of FA oxidation

A

Transfer of fatty acyl-coa into the cell via carnitine acyltransferase 1,2

124
Q

What is the rate limiting step of FA oxidation

A

Carnitine acyltransferase 1,2 (1 on outer membrane, 2 on inner mitochondrial membrane)

125
Q

what is produced from the B-ox of FA

A

FADH2, NADH, actyl-CoA

126
Q

these FA will generate C3 coA to conversion to C4 CoA (succinyl-coa)

A

odd-numbered FA

127
Q

What causes ketogenesis

A

low glucose in the body

128
Q

when there is not enough of this compound acetyl-coa is oxidized into ketoacids

A

oxaloacetate

129
Q

T/F: ketone bodies can’t cross the blood brain barrior, FA can

A

F

130
Q

Ketogenesis is common in these two conditions

A

type 1 diabetics, starvation

131
Q

T/F: ketone bodies are acidic

A

T

132
Q

Ketone bodies make up this percent of fuel during starvation

A

75%

133
Q

T/F: Ketogenesis reaction goes one way in extra hepatic tissues, but is reversable in the liver

A

F

134
Q

This rises during accelerated FAox + low CHo intake or impaired CHO use

A

ketone concentration

135
Q

What role does does ketogenesis p[lay in energy metabolism

A

provides energy that can be used by tissues such as the brain during periods of low blood CHO

136
Q

From what substrate are FA synthesized from

A

acetyl-CoA

137
Q

T/F: pyruvate to acetyl coa is a reversable reaction

A

F

138
Q

What triggers FA synthesis

A

alot of acetyl-coa in the mitochondria

139
Q

this enzyme activates acetyl-coa for FA synthesis

A

acetyl-coa carboxylase

140
Q

this is the basic building block for FA synth

A

malonyl-coa

141
Q

During FA synthesis this energy source is used to get rid of double bonds

A

NADPH

142
Q

This is generally the final product of FA synthesis

A

Palmatic acid

143
Q

How do eicosanoids synthesized from n-6 FA differ from those synthesized from N-3 FA

A

N-6 are pro-arrythmic, platlet activators, vasoconstrictors, pro-inflammatory compounds
n-3 are the opposite

144
Q

There are more of this type of FA in the western diet that make eicosanoids than this

A

n-6 than n-3

145
Q

improved vision, neuroprotection, successful aging, memory protection, cardioprotection, and use as a signaling molecule are all benefits of this type of FA

A

n-3 (DHA)

146
Q

How does CHO balance affect the processes of lipid metabolism

A

more CHO in the system leads to lower catabolism, and greater anabolism of FA

147
Q

T/F: insulin lowers lipolysis activity

A

T (see page 53 of lipid notes)

148
Q

how does brown fat differ from white (normal) fat tissue

A

it is highly vascularized
abundant mitochondria
mitochondria have H+ pores (uncoupling protein) which promote thermogenesis

149
Q

uncoupling protein is inhibited by these

A

free purine nucleotides

150
Q

t/f: lean subjects have higher amounts of brown adipose tissue

A

T

151
Q

Two systems used to metabolize alcohol

A

alcohol dehydrogenase pathway

microsomal ethanol oxidizing system

152
Q

alcohol resembles this compound, but is metabolized like this compound

A

CHO

FA

153
Q

T/F: mass production of Acetyl-coa during ADH alcohol metabolism lowers TCA cycle activity and lends to production of FA

A

T

154
Q

ADH is found here

A

gastric mucosal cells

155
Q

How does alcohol effec energy metabolism in the body

A

alters NADH processes in the body

156
Q

This is tghe cause of the flushing associated with alcohol consumption

A

acetaldehyde

157
Q

Alcohol tolerance is due to this pathway

A

MEOS

158
Q

The benefits of alcohol have the strongest correlation of this and not this

A

amount of alcohol consumed, not the type

159
Q

T/F: alcohol lowers oxidative stress

A

T

160
Q

T/F: alcohol improves insulin sensitivity

A

T

161
Q

T/F: Diabetes is improved from alcohol

A

T

162
Q

T/F: inflammation is increased with alcohol

A

F

163
Q

T/F: alcohol decreases HDL

A

F

164
Q

T/F: dementia is improved with alcohol

A

T

165
Q

T/F: consumption of alcohol may suppress proliferation of smooth muscle cells underlying the endothelium of arterial walls

A

T

166
Q

Outline the progression of atherosclerosis

A

LDL enters intima followed by monocyte
monocyte turns into macrophag and begins to take up LDL
Macrophage dies and froms foam cell
smooth muscle begins to enter intima

167
Q

outline the progression of an athrosclortic lesion

A

fatty streak forms
fibrous cap froms over fatty streak
the fiborous cap thins
eventually the plaque (fiberous cap) bursts froming a thrombus

168
Q

Sites of greatest predilection for atherosclerosis development

A

branching points

169
Q

These two things increase LDL cholesterol

A

SF

TF

170
Q

these three things decrease LDL

A

soluble fiber
plant sterols
saponins

171
Q

This decreases HDL

A

Trans fat

smoking

172
Q

This increases HDL

A 
moderate alcohol (1 to 2 drinks/d depending on sex)
exercise
173
Q

4 parts of the basic amino acid strcuture

A

central carbon
amino group
carbaxy group
side chain

174
Q

What are essential amino acids

A

amino acids needed in the diet because your body cannot make them

175
Q

which amino acids are essential

A 
PVT TIM HaLL
Phenylalanine
Valine
Threonine
Tryptophan
Isoleucine
Methionine
Histidine
Leucine
Lysine
176
Q

Conditionally essential amino acids

A 
Tyrosine
cysteine
proline
arginine
glutamine
177
Q

This AA becomes essential with phenylketonuria

A

tyrosine, unable to produce tyrosine from phenylanine

178
Q

4 levels of protein structure

A

primary
secondary
tertiary
quaternary

179
Q

What protein sources are complete

A

animal
soy
quinua

180
Q

which protein sources are incomplete

A

plant

181
Q

changes 3/d structure of protein, destroys function

A

protein denaturation

182
Q

heat, acid, mechanical force, salt

A

mechanisms of protein denaturation

183
Q

Protein digestion location: pepsin

A

stomach

184
Q

PProtein digestion location: trypsin

A

intestine

185
Q

Protein digestion location: chymotrypsin

A

intestine

186
Q

Protein digestion location: carboxypeptiase A and B

A

intestine

187
Q

Protein digestion location: aminopeptidases

A

intestine

188
Q

products of protein digestion

A

free AA
dipeptides
tripeptides

189
Q

absorption of AA occurs here

A

duodenum

jejunum

190
Q

These AA are absorped most quickly

A

essential AA

191
Q

these AA are absorbed slowly

A

Neg charge

192
Q

This is a cotransporter of AA

A

Na

193
Q

This is how a majority of AA are absorbed, and are faster than AA transporters

A

Peptide transporter

194
Q

T/F: not all di/tri peptidases are all the way broke down before passing into circulation

A

T

195
Q

AA enter this circulation

A

portal

196
Q

The amino acid pool is utilized in these three ways

A

energy production
syntesis of glucose and FA
synthesis of nonprotein molecules that contain nitrogen

197
Q

T/F: the main way to use AA in the body is in the formation of body proteins

A

T

198
Q

Where are amino acids primarily catbolized

A

liver

199
Q

what are the features of sickle cell anemia

A

glu is switched out for valine

200
Q

this structure of hemoglobin is distorted in sickle cell anemia

A

3d (tertiary)

201
Q

What is transamination

A

transfer of amino group from one AA to AA carbon skeleton or a-keto acid

202
Q

what is deamination

A

removal of amino group, no transfer

203
Q

The enzyme responsable for deamination is called this rather than this because the reaction process by loss of elements of water

A

dehydratase

deaminase

204
Q

These are required by dehydratase

A

B6

PLP

205
Q

What is the role of the urea cycle

A

formation of urea (nitrogen containing compound) as a waste product

206
Q

What is the role of the glucose-alanine cycle

A

regeneration of intermediates from AA and transport of N to live

207
Q

how is nitrogen disposed of in the muslce

A

pyruvate is converted to alanine which can leave the muscle and enter circulation, eventually ending up in the liver

208
Q

Functional categories of proteins

A 
catalysts
messengers
structural elements
buffers
fluid balancers
immunoprotectors
transporters
acute phse responders
209
Q

what are the three BCAA

A

valine
leucine
isoleucine

210
Q

in ability to process BCAA and metabolites causing the uring to look and smell like maple syrup

A

maple syrup urine disease

211
Q

T/F: BCAA’s help with muslce building and recovory

A

T

212
Q

AA that is major source of energy for intestinal cells

A

glutamine

213
Q

What are recommended intakes of protein for adults

A

0.8g/kg or 10-35%kcal

214
Q

how does lean muscle mass change throughout the lifetime

A

lean mass increases throughout childhood and adolescence (to age 25) after age 50 there is a 1-2% lose per year

215
Q

How is ammonia handled in the body

A

converted to urea in the liver, and excreated trhough the kidney

216
Q

review starvation v stress in protein, last page of protein notes

A

okay

NUTR-455 (4 decks)

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