Exam 3 Flashcards

(216 cards)

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
T/F: a cholesterol molecule is a steroid molecule with an extra OH, CH3, and FA group attached to it
t
26
What makes a cholesteryl ester different that a cholesterol molecule
cholesteryl ester have a FA bound to the OH group through an ester bond
27
Sex hormones, bile acids, vitamin D, and corticosteroids are made from these
sterols and steroids
28
What is helpful about ingestion of phytosterols
they help eliminate cholesterol through the diet (compete for absorption)
29
These function as emulsifiers, cell membrane and lipoprotein components
phospholipids
30
T/F: phospholipids can interact with polar and non polar compounds
T
31
In most cases the two FA tails on a phospholipid are this type of FA
SFA
32
The hydrophilic portion of a phospholipid is called this
polar head group
33
Phospholipids act as signaling molecules which lead to the activation of this, or the release of this
activation of protein kinase C leading to enzyme activation | release of Ca2+ leading to enzyme activation, or other hormonal responses
34
This is the main phospholipid
lecithin
35
these have a SFA in position 1 and a UFA in position two
glycerophosphatides
36
examples of a glycerophosphatide
lecithin, cardiolipin
37
a type of phospholipid that is abundant in nerve tissue
sphingolipids
38
This are structural lipids in nerves and brain tissue that have a saccaride component
glycolipids
39
Estimated intake of TAG, PL, Chol/phytosterols
100-150 g/d ~5 g/d 200-400 mg/d
40
Fat spoils due to this
oxidation
41
these accelerate oxidation of fat
double bonds
42
these factors limit fat oxidation (4)
limit exposure to air cold temp antioxidants partial hydrogenation
43
This enzyme is used to convert eholesterol esters into cholesterol and FFA
Cholesterol esterase (cholesterol ester hydrolase)
44
How does bile aid in lipid digestion
increases surface area of the lipids, so enzymes can interact
45
How does lingual lipase aid in lipid digestion
it is good at cleaving short chain FA | Turns TAGs into DAGs and FFA
46
This enzyme accounts for 10-30% TAG digestion
gastric lipase
47
Gastric lipase aids lipid digestion by
it is good at cleaving short chain FA | Turns TAGs into DAGs and FFA
48
How does pancreatic lipase aid in lipid digestion
breaks down the ester bonds on the ends of the TAG to from MAGs and 2FFA
49
The majority of lipid digestion occurs here
upper jejunum
50
How does phospholipase A2 aid in lipid digestion
removes the middle FA from a phospholipid forming a FFA and a lysophospholipid
51
a lysophospholipid is this
a digested phospholipid
52
Cholesterol esterase is produced here, and acts on this
pancreatic acinar cells | sterol esters
53
These four compounds are produced by pancreatic acinar cells
cholesterol esterase phospholipase A2 Procolipase pancreatic lipase
54
gastric lipase is produced by this
chief cells of the stomach
55
how does colipase aid in lipid digestion
activates pancreatic lipase
56
Examples of pancreatic lipase inhibitors
orlistat xenical alli
57
why should people take a pancreatic lipase inhibitor
trouble with lipid digestion | weight loss
58
The 5 final products of lipid digestion
``` lysophospholipids nonesterified (free) cholesterol nonesterified (free) FA Nonesterified (free) Plant Sterols 2-Monoglycerides ```
59
This is a way to deliver FA and fat soluble vitamins in an aqueous enviornment
mixed micelles
60
This percent of FA are absorbed in the diet, and this percent of cholesterol
>95% | ~50%
61
This percent of FA in the diet are LCFA
92-96%
62
This carries medium chain fatty acids in the blood
albumin
63
How are SCFA and MCFA absorbed
directly into the capillaries
64
T/F: use medium chain FA if you have a hard time absorbing lipids such as in cystic fibrosis
T
65
This FA length increases energy expenditure after a meal
MCFA
66
The mixed micelle interacts with this
untirred water layer of the brush boarder
67
FFA go here, while the Chylomicron formed from the golgi app. go here
portal vein | lymphatic system
68
most important protein on a chylomicron
apo B-48
69
Chylomicrons from here
distal duodenum and jejunum
70
the majority of the chylomicron is made up of this
triglycerides
71
T/F: LCFA first go to the liver, while SCFA and MCFA first go to systemic circulation
F
72
Chylomicron activity peaks this long after a meal
30 min
73
the lymp system goes to tissues in this order
muscles adipose liver
74
this enzyme is in the adipose, muscle, mammary gland, brain, macrophages, and kupffer cells
lipoprotein lipase (LPL)
75
this enzyme facilitates deposition of FAs in tissues for storage or energy production
lipoprotein lipase (LPL)
76
In this state, activity is high in adipose and low in skeletal and heart muscle for LPL
fed state
77
In this state, activity is low in adipose and high in skeletal and heart muscle for LPL
fasted
78
These carry absorbed dietary lipids, carry lipids from liver to cells, and carry lipids to liver for excretion
lipoproteins
79
examples of lipoproteins (4)
chylomicron VLDL LDL HDL
80
characteristic apoprotein for VLDL
apo B-100
81
characteristic apoprotein for LDL
apo B-100
82
characteristic apoprotein for HDL
apo A-I
83
These act as identification, stablizie, specificity, and aid in recognition of lipoproteins
apoproteins
84
chylomicrons originate here
golgi app of intestinal cells
85
chylomicrons are composed of
mostly TAG with little phospholipid, cholesterol and protein
86
VLDL originate here
liver (golgi app)
87
VLDL are composed of
mostly TAG with a little more phospholipids, cholesterol, and protein than chylomicrons
88
carry lipids from liver to cells, deliver TG to cells then shrink to become IDL
VLDL
89
LDL originate from this
IDL
90
LDL are taken up by this
B-100 receptors fround in the liver and hon-hepatic tissue
91
These are generated from the VLDL during circulation, carry lipids to cells, mainly carry cholesterol (large proportion), uptaken by LDL receptor
LDL
92
Chylomicrons follow this pathway, while VLDL and IDL follow this pathway
exogenous | endogenous
93
T/F: the more cholesterol in the cell, the less LDL receptors are formed
T
94
This occurs when LDL is absorbed in the cell
lysosome digests | free cholesterol is packaged by the golgi app, and esterified with ACAT and stored in the cell
95
exogenous lipids (gut to liver)
chylomicron
96
endogenous lipids (liver to periphery)
VLDL | LDL
97
reverse transport (periphery to liver)
HDL
98
synthesized from liver and intestine in a lipid free nascent form
HDL
99
Mostly protein composes its structure
HDL
100
This LP returns lipids (cholesterol) to liver for re-use or excretion
HDL
101
T/F: there are smaller fluctuations in LDL and HDL concentrations in the blood than in CM, VLDL, IDL
T
102
This tissue synthesizes bile salts, VLDL, HDL, and new lipids from non-lipid precursors
Liver
103
this tissue absorbs TAG and cholesterol from chylomicrons through lipoprotein lipase, and stores TAG
adipose tissue
104
What is lipoprotein lipase
found on adipose and muscle tissue, removes FA from TAGS in chylomicrons and VLDL and brings them into the cell
105
this helps to transfer cholesterol to the liver and eventually excrete it
cholesterol ester transfer protein
106
This percent of adipose tissue is lipid material
85%
107
HDL acts inconjuction with these two enzymes to move cholesterol from the peripheral tissues to the liver via the plasma
cholesterol esterifying enzyme | lecithin: cholesterol acyltransferase (LCAT)
108
these are cholesterol delivery trucks, and increase risk of CVD
LDL
109
these are cholesterol garbage trucks and perform reverse cholesterol transport, decrease risk of CVD
HDL
110
Chylomicrons are made here
enterocytes
111
secretion of chylomirons
exogenous, intestinal cell to lymph, to blood
112
chylomicrons change to this during dirculation
chylomicron remnant
113
physiological role of chylomicrons
deliver FA to the peripheral cells (adipocytes)
114
Key enzyme in cholesterol synthesis
HMG-CoA reductase
115
What is the rate-limiting step of cholesterol synthesis
HMG-CoA reductase
116
where are VLDL and LDL synthesized
hepatocytes
117
where is HDL synthesized
hepatocytes (80%) enterocytes (20%)
118
earliest stage of HDL
nascent HDL
119
First step of FA metabolism
extract lipids from LP via LPL (lipoprotein lipase)
120
the cleavage of a staturated CC bond during FAox yields this many ATP
5
121
Glycerol cannot be utilized by the cell, so it is sent here
liver
122
Phase 1 of FA oxidation
activation of FA by CoA (acyl-CoA synthetase) forms Acyl-CoA
123
Phase 2 of FA oxidation
Transfer of fatty acyl-coa into the cell via carnitine acyltransferase 1,2
124
What is the rate limiting step of FA oxidation
Carnitine acyltransferase 1,2 (1 on outer membrane, 2 on inner mitochondrial membrane)
125
what is produced from the B-ox of FA
FADH2, NADH, actyl-CoA
126
these FA will generate C3 coA to conversion to C4 CoA (succinyl-coa)
odd-numbered FA
127
What causes ketogenesis
low glucose in the body
128
when there is not enough of this compound acetyl-coa is oxidized into ketoacids
oxaloacetate
129
T/F: ketone bodies can't cross the blood brain barrior, FA can
F
130
Ketogenesis is common in these two conditions
type 1 diabetics, starvation
131
T/F: ketone bodies are acidic
T
132
Ketone bodies make up this percent of fuel during starvation
75%
133
T/F: Ketogenesis reaction goes one way in extra hepatic tissues, but is reversable in the liver
F
134
This rises during accelerated FAox + low CHo intake or impaired CHO use
ketone concentration
135
What role does does ketogenesis p[lay in energy metabolism
provides energy that can be used by tissues such as the brain during periods of low blood CHO
136
From what substrate are FA synthesized from
acetyl-CoA
137
T/F: pyruvate to acetyl coa is a reversable reaction
F
138
What triggers FA synthesis
alot of acetyl-coa in the mitochondria
139
this enzyme activates acetyl-coa for FA synthesis
acetyl-coa carboxylase
140
this is the basic building block for FA synth
malonyl-coa
141
During FA synthesis this energy source is used to get rid of double bonds
NADPH
142
This is generally the final product of FA synthesis
Palmatic acid
143
How do eicosanoids synthesized from n-6 FA differ from those synthesized from N-3 FA
N-6 are pro-arrythmic, platlet activators, vasoconstrictors, pro-inflammatory compounds n-3 are the opposite
144
There are more of this type of FA in the western diet that make eicosanoids than this
n-6 than n-3
145
improved vision, neuroprotection, successful aging, memory protection, cardioprotection, and use as a signaling molecule are all benefits of this type of FA
n-3 (DHA)
146
How does CHO balance affect the processes of lipid metabolism
more CHO in the system leads to lower catabolism, and greater anabolism of FA
147
T/F: insulin lowers lipolysis activity
T (see page 53 of lipid notes)
148
how does brown fat differ from white (normal) fat tissue
it is highly vascularized abundant mitochondria mitochondria have H+ pores (uncoupling protein) which promote thermogenesis
149
uncoupling protein is inhibited by these
free purine nucleotides
150
t/f: lean subjects have higher amounts of brown adipose tissue
T
151
Two systems used to metabolize alcohol
alcohol dehydrogenase pathway | microsomal ethanol oxidizing system
152
alcohol resembles this compound, but is metabolized like this compound
CHO | FA
153
T/F: mass production of Acetyl-coa during ADH alcohol metabolism lowers TCA cycle activity and lends to production of FA
T
154
ADH is found here
gastric mucosal cells
155
How does alcohol effec energy metabolism in the body
alters NADH processes in the body
156
This is tghe cause of the flushing associated with alcohol consumption
acetaldehyde
157
Alcohol tolerance is due to this pathway
MEOS
158
The benefits of alcohol have the strongest correlation of this and not this
amount of alcohol consumed, not the type
159
T/F: alcohol lowers oxidative stress
T
160
T/F: alcohol improves insulin sensitivity
T
161
T/F: Diabetes is improved from alcohol
T
162
T/F: inflammation is increased with alcohol
F
163
T/F: alcohol decreases HDL
F
164
T/F: dementia is improved with alcohol
T
165
T/F: consumption of alcohol may suppress proliferation of smooth muscle cells underlying the endothelium of arterial walls
T
166
Outline the progression of atherosclerosis
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
outline the progression of an athrosclortic lesion
fatty streak forms fibrous cap froms over fatty streak the fiborous cap thins eventually the plaque (fiberous cap) bursts froming a thrombus
168
Sites of greatest predilection for atherosclerosis development
branching points
169
These two things increase LDL cholesterol
SF | TF
170
these three things decrease LDL
soluble fiber plant sterols saponins
171
This decreases HDL
Trans fat | smoking
172
This increases HDL
``` moderate alcohol (1 to 2 drinks/d depending on sex) exercise ```
173
4 parts of the basic amino acid strcuture
central carbon amino group carbaxy group side chain
174
What are essential amino acids
amino acids needed in the diet because your body cannot make them
175
which amino acids are essential
``` PVT TIM HaLL Phenylalanine Valine Threonine Tryptophan Isoleucine Methionine Histidine Leucine Lysine ```
176
Conditionally essential amino acids
``` Tyrosine cysteine proline arginine glutamine ```
177
This AA becomes essential with phenylketonuria
tyrosine, unable to produce tyrosine from phenylanine
178
4 levels of protein structure
primary secondary tertiary quaternary
179
What protein sources are complete
animal soy quinua
180
which protein sources are incomplete
plant
181
changes 3/d structure of protein, destroys function
protein denaturation
182
heat, acid, mechanical force, salt
mechanisms of protein denaturation
183
Protein digestion location: pepsin
stomach
184
PProtein digestion location: trypsin
intestine
185
Protein digestion location: chymotrypsin
intestine
186
Protein digestion location: carboxypeptiase A and B
intestine
187
Protein digestion location: aminopeptidases
intestine
188
products of protein digestion
free AA dipeptides tripeptides
189
absorption of AA occurs here
duodenum | jejunum
190
These AA are absorped most quickly
essential AA
191
these AA are absorbed slowly
Neg charge
192
This is a cotransporter of AA
Na
193
This is how a majority of AA are absorbed, and are faster than AA transporters
Peptide transporter
194
T/F: not all di/tri peptidases are all the way broke down before passing into circulation
T
195
AA enter this circulation
portal
196
The amino acid pool is utilized in these three ways
energy production syntesis of glucose and FA synthesis of nonprotein molecules that contain nitrogen
197
T/F: the main way to use AA in the body is in the formation of body proteins
T
198
Where are amino acids primarily catbolized
liver
199
what are the features of sickle cell anemia
glu is switched out for valine
200
this structure of hemoglobin is distorted in sickle cell anemia
3d (tertiary)
201
What is transamination
transfer of amino group from one AA to AA carbon skeleton or a-keto acid
202
what is deamination
removal of amino group, no transfer
203
The enzyme responsable for deamination is called this rather than this because the reaction process by loss of elements of water
dehydratase | deaminase
204
These are required by dehydratase
B6 | PLP
205
What is the role of the urea cycle
formation of urea (nitrogen containing compound) as a waste product
206
What is the role of the glucose-alanine cycle
regeneration of intermediates from AA and transport of N to live
207
how is nitrogen disposed of in the muslce
pyruvate is converted to alanine which can leave the muscle and enter circulation, eventually ending up in the liver
208
Functional categories of proteins
``` catalysts messengers structural elements buffers fluid balancers immunoprotectors transporters acute phse responders ```
209
what are the three BCAA
valine leucine isoleucine
210
in ability to process BCAA and metabolites causing the uring to look and smell like maple syrup
maple syrup urine disease
211
T/F: BCAA's help with muslce building and recovory
T
212
AA that is major source of energy for intestinal cells
glutamine
213
What are recommended intakes of protein for adults
0.8g/kg or 10-35%kcal
214
how does lean muscle mass change throughout the lifetime
lean mass increases throughout childhood and adolescence (to age 25) after age 50 there is a 1-2% lose per year
215
How is ammonia handled in the body
converted to urea in the liver, and excreated trhough the kidney
216
review starvation v stress in protein, last page of protein notes
okay