Exam 3 Flashcards
(240 cards)
1
Q
Most fat from food comes in the form of __________
A
triglycerides
2
Q
What class of enzyme hydrolyzes trglycerides into fatty acids?
A
lipases
3
Q
In the fed state, where do fatty acids from food go?
A
adipose tissue
4
Q
In the fasting state, where does the stored fatty acids go?
A
liver and muscles
5
Q
Fatty acids are _____________ molecules because they have both a hydrophobic and hydrophilic moiety
A
amphipathic
6
Q
In the blood fatty acids are bound to __________. Why?
A
Albumin
They are too acidic on thier own
7
Q
What are the steps of fatty acids entering the cell—> mitochondria?
A
- FA transporter at plasma membrane lets FA into cell
- FA is bound to FBP (FA binding protein) in cytosol
- FA is transported into mitochondria
8
Q
Most fatty acids are oxidized in the ______________
A
mitochondria
9
Q
What 2 things are required for the uptake of fatty acids into the mitochondria?
A
- FA binds to CoA = fatty acyl CoA
- fatty acyl CoA binds to carnitine = fatty acyl-Carnitine
10
Q
The uptake of fatty acids into the mitochondria is regulated by the concentration of cytoplasmic ________________
A
malonyl-CoA
11
Q
Is carnitine derived de novo or through the diet?
A
diet
12
Q
Does malonyl coA inhibit or promote the uptake of fatty acids in to mitochondria?
A
inhibit (represses entry)
13
Q
Insulin (through malonyl-coA) inhibits or stimulates FA uptake into mitochondria IN THE LIVER?
A
inhibits uptake
14
Q
AMP inhibits or stimulates FA uptake into mitochondria IN ALL TISSUES?
A
stimulates uptake
15
Q
What is the purpose of beta-oxidation?
A
FA are broken down to generate acetyl-coA and FADH2/NADH
16
Q
How long will the B-oxidation cycle go?
A
until only 2 carbons are left
17
Q
Which carbon is always oxidized in B-oxidation?
A
beta carbon
18
Q
How many carbons are removed per cycle of B-oxidation?
A
2
19
Q
Every 2 carbons removed in the B-oxidation cycle, how many FADH2 is yielded?
A
1
20
Q
Every 2 carbons removed in the B-oxidation cycle, how many NADH is yielded?
A
1
21
Q
Every 2 carbons removed in the B-oxidation cycle, how many acetyl coA is yielded?
A
1
22
Q
What does one round of B-oxidation cost?
Where does it come from?
A
1 ATP
attaching coA to FA
23
Q
How do you find out how many cycles a certain FA will require of B-oxidation?
A
(n/2 -1) = # cycles
n = number of carbons
24
Q
How do you find out how many acetyl-coAs are made from a certain FA undergoing B-oxidation?
A
cycles + 1
25
What is the final carbon product of B-oxidation?
Where does it go?
acetyl coA
Krebs cycle
26
Where does B-oxidation NOT occur?
brain and RBC
(no mitochondria)
27
Where does B-oxidation occur?
mitochondria
28
What are the two sources of acetyl coA?
fed: comes from pyruvate
fasting: comes from B-oxidation (much more of this)
29
Does insulin inhibit or stimulate lipolysis/B-oxidation?
inhibit
30
Does epinephrine inhibit or stimulate lipolysis/B-oxidation?
stimulate
31
When muscles need energy, FA ________ are incorporated into the plasma membrane to uptake FA from blood
FA transporters
32
What are the steps of lipolysis?
1. triglycerides
2. FA + glycerol
3. fatty acyl-coA
4. acetyl coA ---> Krebs cycle
33
What is the purpose of ketone body synthesis?
alternative source of energy besides glucose
34
What are the 3 ketone bodies?
acetoacetate
B-hydroxybutyrate
acetone
35
Do ketone bodies alkalize or acidify blood?
acidify
36
What organ does ketone body synthesis occur?
liver
37
Excess _______________ built up in the mitochondria can be used to synthesize ketone bodies
acetyl coA
38
Is excess acetyl coA from diet or de novo used to make ketone bodies?
de novo (liver mitochondria)
39
What state are ketone bodies made in?
extended fasting
40
Are ketone bodies synthesized during high or low rate of lipolysis? and why
High rate
lots of excess acetyl coA being made from B-oxidation
41
How many acetyl coAs are required to make 1 acetoacetate?
2
42
What are the reactants and products of ketone body synthesis?
2 acetyl coAs ---> acetoacetate + acetone + B-hydroxybutryate
43
The synthesis of ketone bodies after 3 days of fasting induces a _______________ as a safety mechanism
feedback loop
44
The ketone body feed back loop stimulates __________ secretion to impair lipolysis
insulin
45
Why is the ketone body feedback loop in place?
prevent blood from becoming too acidic
46
If ketone bodies induce a feedback loop due to insulin the rate of lipolysis is _______ and the rate of ketogenesis is _______
low
low
47
What does the ketone body feedback loop prevent?
ketoacidosis
48
What is ketone body oxidation?
(ketolysis) break down of ketone bodies
49
What are ketone bodies broken down into and where do they go?
acetyl coA
CAC cycle
50
What tissues use ketone bodies?
brain
heart
muscle
kidneys
51
What tissues don't use ketone bodies?
liver
RBC
52
Cells that oxidize ketone bodies have an increased or decreased need for oxidation of glucose (breakdown of glucose)
decreased
53
Ketolysis = increased/decreased acetyl coA = increased/decreased PDH activity = preserve glucose for brain
increase acetyl coA
decrease PDH
54
Does ketone body oxidation (lysis) inhibit or activate PDH and glycolysis?
inhibit
55
In the fed state the brain uses _____% of glucose.
In the long term fasting state the brain uses ____% ketone bodies
100% glucose
75% ketone bodies
56
What organ cannot oxidize ketone bodies?
Why?
liver
acetyl coA from ketolysis cannot be used in gluconeogensis as a carbon skeleton
57
Where does the energy for gluconeogenesis come from in the liver?
B-oxidation
58
What is it called when B-oxidation and ketolysis inhibits glycolysis?
glucose sparing (for the brain)
59
What are the two ways to slow down glycolysis via B-oxidation and ketolysis?
1. ATP produced from B-oxidation and ketolysis inhibits glycolysis
2. Acetyl coA produced from B-oxidation inhibits PDH
60
What is ketosis?
synthesis of ketone bodies when fasting for 2-3 days
61
What does ketosis shut off and how?
represses lipolysis
secretes insulin
62
What is ketoacidosis?
too much ketone body synthesis and too little degradation acidifies the blood
63
What kind of patients is it common for ketoacidosis to occur?
server insulin deficiency
64
What condition are required for diabetic ketoacidosis?
? [glucose]
? [insulin]
? [ketones]
? pH
[glucose] - high
[insulin] - low
[ketones] - high
pH - low
65
What are the conditions for ketotic hypoglycemia?
? [ketone bodies]
? [glucose]
[ketone bodies] - high
[glucose] - low
66
Ketotic hypoglycemia manifests when there is low/high insulin the the blood
low
67
What are the conditions for non-ketotic hypoglycemia?
? [ketone bodies]
? [glucose]
[ketone bodies] - low
[glucose] - low
68
non-ketotic hypoglycemia manifests when there is low/high insulin the the blood
high
69
Where does the ETC occur?
mitochondria
- inner membrane space
- inner membrane
- matrix
70
Where are the ETC complexes located?
inner membrane of mitochondria
71
What are the 2 mobile electron carriers of the ETC?
coenzyme Q
cytochtome
72
What is complex I of ETC called?
NADH DH
73
Complex I of ETC...
oxidizes ____ to _____
produces _____
NADH to NAD+
Ubiquinol
74
What is the only ETC complex that does not pump a proton?
complex II (Succinate DH)
75
What is complex II of the ETC called?
Succinate DH
76
Complex II of the ETC...
oxidizes _____ to ______
produced ________
FAHD2 to FAD+
Ubiquinol
77
What is complex III of the ETC called?
cyt bc1 complex
78
Complex III of the ETC...
oxidizes ______
transfers e- to _______
ubiquinol
cyt C
79
What is complex IV of the ETC called?
cyt C oxidase
80
Complex IV of the ETC...
transfers e- to _____ generating _______
O2
water
81
In the ETC, where does the proton motive force (PMF) occur?
inner membrane space
protons are pushed into ATPase
82
The inner mitochondrial membrane is permeable or impermeable?
impermeable
83
What is complex V of the ETC called?
F0F1 ATP synthase
84
What is the chemisomotic-coupling hypothesis?
oxidation of NADH and FADH2 is couple with the transport of H+ out of the matrix into the inner membrane space and that gradient drive H+ into ATPase
85
What is the net ATP product of the ETC?
#1 oxidation of 1 NADH = ____ ATP
#2 oxidation of 1 FADH2 = _____ ATP
NADH -- 3 ATP
FADH2 -- 2 ATP
86
ATP production is larger from break down of carbs (glucose) or fats?
fats
87
_____ is the most important factor controlling the rate of oxidative phosphorylation
ADP
88
ATP consumption is high or low when...
ETC doesn't pump H+
NADH grows slowing CAC
ATP synthase makes low ATP
low consumption
89
ATP consumption is high or low when...
ADP increases
ATP synthase makes ATP
CAC increases
high consumption
90
What are the 2 families of ETC inhibitors?
1. targets complex I (NADH DH)
2. targets complex IV (cyt c oxidase)
91
ETC inhibitors make the body hot or cold?
cold
92
What is an example of complex I inhibitor of ETC?
metformin
93
Metformin lowers ________ in the blood
glucose
94
Metformin can cause ___________ because of the increase in anaerobic glycolysis
lactic acidosis
95
How do complex IV (cyt c oxidase) inhibitors work?
bind to heme
96
How do uncouplers of the ETC work?
collapse the pH gradient causing H+ to cross back making complexes go faster
97
ETC uncouplers cause the body to become hot or cold?
hot
98
How do you interpret this fatty acid to be?
16:2
16 carbons
2 double bonds
99
How do you name carbons with the alternative method?
start number carbons at the CH3 end of the chain
99
How do you name fatty acids using the standard method?
start number carbons at the carbonyl carbon
100
Do saturated FA have a double bond?
no
101
Do unsaturated FA have a double bond?
yes
102
Saturated fats tend to be solid or liquid at room temperature?
solid (animal products)
103
Unsaturated fats tend to be solid or liquid at room temperature?
liquid (plant products)
104
Do saturated or unsaturated FA can come in trans and cis?
unsaturated
105
The human body can only synthesize cis or trans unsaturated FA but can degrade both?
cis
106
Cis FA tend to be liquid or solid?
liquid
107
Trans FA tend to be liquid or solid?
solid
108
In the standard method of naming fats, what does the delta mean?
double bond position
109
What are the 3 essential fatty acids?
1. linoleate (w-6)
2. linolenate (w-3)
3. arachidonate
110
What 2 fatty acids are used as supplements?
EPA (w-3)
DHA (w-3)
111
Free fatty acids are toxin in high concentrations because they are so acidic. What are they bound to to neutralize them?
albumin
112
Inside of cells fatty acids are bound to ________ instead of albumin to neutralize them
FABPs
113
What are the 4 general steps of FA synthesis?
1. citrate movement from mitochondria (CAC) to cytoplasm of hepatocytes (liver cells)
2. production of cytoplasmic acetyl coA (from citrate)
3. production of malonyl coA
4. FA synthesis via FA synthase
114
Where does FA synthesis occur?
liver
115
Metabolic conditions that allow citrate to leave CAC (mitochondria) for FA synthesis are...
_____ insulin
_____ PFK1
glucose -----> ______
pyruvate into _______
increased insulin
increased PFK1 activity
glucose -----> pyruvate
pyruvate ----> CAC
116
Does insulin stimulate or inhibit FA synthesis?
stimualte
117
In FA synthesis, citrate leaves the mitochondria and turns into ___________
acetyl coA
118
In FA synthese, after citrate is turned into acetyl coA, what does it become next?
malonyl coA
119
What enzyme turns acetyl coA into malonyl coA in FA synthesis?
acetyl coA carboxylase
120
Does insulin inhibit or activate acetyl-coA carboxylase?
activates (promotes FA synthesis)
121
Where do the first 2 carbons needed for FA synthesis come from?
acetyl CoA
122
Each 2 carbon addition during FA synthesis costs ____ NADPH and ____ ATP
2 NADPH
1 ATP
123
How many NADPHs are required for synthesizing a C16?
14
2x7rounds
124
How many ATP are needed to synthesize C16?
7
(acetyl coA --> malonyl CoA)
125
How many acetyl coA are needed to synthesize a C16?
8
(1 primer + 7 malonyl coA)
126
What are the two sources of NADPH for FA synthesis in the liver?
1. PPP (2 NADPH per glucose)
2. Malate DH (1 NADPH per malate)
127
Regular FA synthesis goes only up to C___, anything longer than that has to be syntheized by ______________
16
elongation
128
What are the 2 steps of FA elongation?
1. activation via esterification
2. elongation
129
What is desaturation of FAs?
addition of double bonds
130
What 2 molecules are required for FA desaturation?
O2
NADH
131
What is the limitation of desaturation of FA in humans?
desaturase can only introduce double bonds between carbon atoms 1-9
132
FAs that contain 2 or more double bonds after carbon 9 come from diet making them ______________
essential
133
What are the two types of essential fatty acids?
1. Linoleate (w-6)
2. Linolenate (w-3)
134
The body converts ___________ to EPA and DHA (supplements)
linolenate (w-3)
135
The body converts _________ to arachidonate
linoleate (w-6)
136
What is the supplement DHA important for?
brain and retina
137
What are eicosanoids?
stores arachidonic acid
137
138
What is the purpose of prostaglandins?
inflammation
139
NSAIDs like aspirin inhibit ___________ enzyme
COX 1 & 2
140
What are the 2 functions of inhibition of aspirin?
1. inhibits prostaglandin (reduce inflammation)
2. inhibits thromboxane (anticoagulant)
141
What are the major sources of trans fats?
animal meat
heated cis fats
chemically hydrogenated fats
142
What are lipoproteins?
large assembly of molecules made of proteins and lipids that transport lipids
143
What are the 4 major lipid classes?
1. triglycerides
2. cholesteryl esters
3. cholesterol
4. free FAs
144
What are the 5 major groups of plasma lipoproteins?
1. chylomicrons
2. VLDL
3. IDL
4. LDL
5. HDL
145
What are the 2 "bad" lipoproteins?
IDL
LDL
146
Chylomicrons and VLDL are mainly made of ___________
lipids
147
Cholestrol and phospholipids (IDL, LDL, and HDL) are mainly made of _____________
proteins
148
What are the 2 chemical properties of lipoproteins?
1. density
2. size
149
Are chylomicrons or HDL lighter?
chylomicrons
150
What's the heaviest lipoprotein?
HDL
151
What are the proteins present in lipoproteins called?
Apo
152
Why is ApoB-100 important?
marker for bad cholesterol (LDL)
152
What kind of Apo is ApoB-100?
exchangeable or non-exchangeable?
non-exchangeable
153
Where are chylomicrons originated and VLDL?
1. dietary lipids (chylomicrons)
2. lipid synthesis (VLDL)
154
What makes VLDL different from chylomicrons composition?
VLDL has much more cholesterol esters
155
Chylomicrons and VLDL are hydrolyzed of thier triacylglycerol by ______________
lipoprotein lipase
156
What are the 5 steps of the fate of chylomicrons?
1. fat uptake from diet
2. chylomicron synthesis
3. removal of FAs
4. enrichment in cholestrol/loss of triacylglycerol
5. liver uptakes remnants via LDL receptor-related protein
157
What are the 5 steps of the fate of VLDL?
1. Fat synthesis in liver
2. VLDL synthesis
3. removal of FAs
4.enrichment in cholestrol/loss of triacylglycerol
5. liver uptakes remnant (LDL)
158
Is chylomicron remnants or LDL richer in cholesterol?
LDL
159
Lipoprotein lipase deficiency leads to ________- triglyceridemia
hyper (elevated triglycerides in blood)
160
What 2 things does HTGL (hepatic lipase) do?
converts VLDL into IDL
remodels large HDLs into smaller ones
161
What hormone controls lipoprotein lipase and how?
insulin
stimulates LPL activity in ADIPOCYTES
inhibits LPL in MUSCLES
162
What happens to chylomicrons after lipolysis?
remnants taken up by liver (endocytosis)
163
What happens to VLDL after lipolysis?
degraded to IDL and LDL and taken up by liver
164
How is LDL metabolized into the liver?
LDL receptor
165
Recognition of LDL via LDL-r is mediated by _______
B-100
166
What is reverse cholesterol transport?
HDL removes fat molecules form cells because they cannot do it themselves
167
What 2 things are HDL very important for?
1. HDL removes cholesterol from arterial walls
2. high levels of HDL protect against atherosclerosis
168
What does LCAT do in HDL metabolism?
converts free cholestrol into cholesteryl esters which is taken up by HDL
169
What is CETP important for in HDL metabolism?
collects triglerides from VLDL/LDL and exchanges them for cholesteryl esters from HDL
170
What is PLTP important for in HDL metabolism?
transfers phospholipids from lipoproteins to HDL
171
LCAT is bound to ____ and _____ in the blood
LDL and HDL
172
What molecule does cholesterol look like?
steroids
173
What are the 2 important carbons on cholesterol?
C3 - hydroxyl group (site of esterfication)
C17 - aliphatic chain
174
where does cholesterol come from?
de novo
diet
175
Where do all the carbon atoms of cholesterol come from?
acetyl coA
176
It costs ______ acetyl coA and ____ ATP per 1 cholesterol?
18 acetyl coA
36 ATP
177
Where does the acetyl coA that goes into cholesterol come from?
mitochondrion citrate
178
Where in the cell does cholestrol synthesis take place?
cytoplasm and ER
179
What organ does most of cholesterol synthesis take place in?
liver
180
Whats the difference between cholesterol and cholesterol esters?
esters have a FA side on the C3
181
What is the main purpose of cholesterol esters?
storage and transport of cholestrol
182
What are the two pathways of cholesterol ester synthesis and the enzyme used?
1. in tissues (ACAT)
2. in plasma *LCAT)
183
Break down of cholesterol esters make what and is done by what enzyme?
cholesterol and FA
esterases
184
What are the 3 types of esterases?
1. pancreatic cholesterol easterases
2. lysosomal acid cholesteryl hydrolase
3. NCEH
185
What is the purpose of cholesterol?
changes membrane fluidity
186
187
What are the 4 types of membranes containing cholesterol and rank them from least to most cholesterol.
1. ER, Golgi, mitochondria (most fluid)
2. plasma membrane
3. RBC membrane and nerve cells
4. cell membrane of eye lens (stiff)
188
What are 3 important derivatives of cholesterol?
1. bile acid
2. vitamin D1
3. steroids
189
What is the equation for [LDL]?
total - HDL - TG/5
190
What are 3 ways to reduce cholesterol uptake?
1. diet
2. additives
3. weight loss/exercise
4. statins
191
Statins are competitive inhibitors of __________________
HMG coA reductase
192
________ must be ingested for the synthesis of AAs, proteins, neurotransmitters, nucleotides and ATP
nitrogen
193
What is the limitation of nitrogen?
it cannot be stored in the body
194
What are the 2 reactions that convert ammonium (NH4+) into organic nitrogen?
1. a-ketogluterate + NH4+ ------> glutamate
2. glutamate + NH4+ -----> glutamine
195
What enzyme catalyzes a-ketogluterate + NH4+ ------> glutamate?
glutamate DH
196
What enzyme catalyzes glutamate + NH4+ -----> glutamine?
glutamine synthetase
197
Is glutamine or glutmate toxic?
glutamate
198
What are the 3 roles of amino acids in metabolism?
1. protein synthesis
2. fuel source
3. precursor for biosynthesis
199
What are the 3 sources of amino acids?
1. breakdown of body protein
2. AA from diet
3. biosynthesis from other metabolites
200
What are the 3 classifications of amino acids?
1. glucogenic
2. ketogenic
3. amphibolic
201
What does it mean if an amino acid is classified as glucogenic?
gives rise to glucose via conversion of pyruvate/TCA intermediate
202
What does it mean if an amino acids is classified as ketogenic?
gives rise to acetyl coA
203
What are the 9 essential amino acids?
Arg
His
Ile
Leu
Thr
Lys
Met
Phe
Trp
Val
(Any Help In Learning These Little Molecules Proves Truly Valuable)
204
What are non-essential amino acids?
can be synthesized in the body
205
What is nitrogen balance?
the uptake and degradation of nitrogen must be equal
206
What is positive nitrogen balance? What are 3 scenarios?
taking up more than you can degrade
1. growing children
2. pregnancy
3. tissue repair
207
What is negative nitrogen balance?
more degradation that uptake
208
What are 3 examples of negative nitrogen balance?
1. trauma/stress
2. marasmus
3. kwashiorkor
209
In negative nitrogen balance, Marasmus has prolonged deficiency in ______ and _______
protein
caloric intake
210
In negative nitrogen balance, Kwashiorkor has prolonged deficiency in ______ but not _______
protein
caloric intake
211
What are 2 ways proteins can be degraded by cells?
lysosomes (cytoplasm)
proteasomes (cytoplasm/nucleus)
212
How are proteins targeted to proteasomes for degradation?
marked with poly-ubiquitin tag
213
Where does protein degradation start and continue?
stomach via juices and proteases
pancreas and small intestines
214
What 2 ways do digested proteins enter the blood stream as amino acids/small peptides?
1. Na+ dependent transport
2. just cross the lining
215
What are the 2 steps in the 1st step of amino acid catabolism?
1. transamination
2. oxidative deamination
216
Where are amino acids degraded?
muscle and liver
217
What is the first step of amino acids catabolism?
removal of alpha-amino group (transamination then ox. deamination)
218
What occurs in the transamination step of amino acid catabolism?
alpha-amino group of AA is transferred to a-keto acid to form glutamate
219
What occurs in the oxidative deamination step of amino acid catabolism?
glutamate is deaminated to yield NH4+
220
why does glutamate play a central role in amino acid catabolism?
controls the nitrogen levels
221
Transamination and oxidative deamination of AAs is a ___________ reaction
coupled
222
What enzyme catalyzes transamination/oxidative deamination?
glutamate DH
223
What 2 molecules inhibit glutamate DH?
GTP and ATP
224
Where does the urea cycle occur?
cytoplasm and mitochondria
225
Where do the 2 nitrogens and the carbon from urea come from?
1. a free ammonia
2. amino group of aspartate
1. CO2
226
What is the first step in the urea cycle and what is it catalyzed by?
NH3 + CH3O ----> carbamoyl phosphate
CPS-1
227
How many ATP does the first step of the urea cycle cost?
2
228
What is the rate limiting step of the Urea cycle?
1st
CPS-1
229
The activity of CPS-1 in the urea cycle is dependent on ___________
NAG
230
The concentration of __________ determines the rate and activity of the urea cycle
NAG
231
What is NAG formed from in the urea cycle?
acetyl coA
232
NAG synthase in the Urea cycle is activated by _________
arginine
233
Activation of the urea cycle via stimulation of carbamoyl phosphate synthase -1 (CPS-1) occurs only when there is ...
#1
#2
#3
#1 NH3 to maintain glutamate levels
#2 acetyl CoA + glutamate to make NAG
#3 arginine to activate NAH synthase
234
How is the urea cycle and the TCA cycle interlinked?
aspartate goes from TCA to urea and fumarate comes out of urea cycle and into TCA
235
Any defect in urea synthesis results in _____________
hyperammonemia
236
What are the 2 main causes of urea cycle defects?
liver disease
genetic defects
237
How is lactulose used as a treatment for urea cycle disorders?
reduces ammonia in blood
gut bacteria ferment the lactulose and will acidify the gut which allows NH3 from blood to enter gut and protonate into NH4+ and is peed out
