EXAM 3 Flashcards
(469 cards)
1
Q
Lipid digestion is mainly
A
triacylglycerols (90%)
2
Q
10% of lipid digestion is
A
cholesterol, cholesteryl estres, phospholipids, and free fatty acids
3
Q
what are the important enzymes for lipid digestion
A
pancreatic lipase
colipase
cholesterol esterase
4
Q
what are the three sections of lipid metabolism
A
digestion
absorption
transport
5
Q
T/F In lipid digestion it is possible for micelle formation
A
T
6
Q
In lipid absorption what occurs
A
formation of chylomicrons
7
Q
List the different lipoproteins
A
chylomicrons
VLDL
LDL
IDL
HDL
8
Q
what are the major form of energy storage in humans
A
triacylglycerols
9
Q
The oxidation of fatty acids occurs in a repetitive four step process known as
A
β-oxidation
10
Q
The processing of dietary lipids (which is primarily fats) occurs in 8 steps:
A
- Bile salts mix with fats in the small intestines to form mixed micelles
- Intestinal lipases degrade triacylglycerols to form the products of fatty acids and glycerol
- Fatty acids are taken up by the intestinal mucosa and converted into triacylglycerols
- Reconverted triacylglycerols are packaged with dietary cholesterol to from lipoprotein
aggregates called chylomicrons. - Chylomicrons are shuttled through the lymph system and the blood stream to various tissues.
- In the capillaries, extracellular lipoprotein lipase is activated by apoC-II to hydrolyze the
fatty acids and glycerol. - The fatty acids and glycerol are then taken up by cells.
- In muscle cells the fatty acids can be used, in adipocytes they are reesterfied for storage
as triacylglycerols.
11
Q
Triacylglycerols are ____________ and thus must first be ___________ before they can be digested
A
insoluble
emulsified
12
Q
define emulsification
A
the process by which fat globules are broken down into
droplets,
13
Q
emulsification is facilitated by
A
bile salts and lipases
14
Q
Bile salts/Bile acids are what kind of molecules and where are they synthesized and from what are they synthesized
A
amphiphilic molecules synthesized
from cholesterol in liver
15
Q
Bile salts or bile acids are stored in and where are they released ?
A
the gall bladder
released into the small intestines for digestion purposes
16
Q
T/F enzymes operate in an insoluble environment
A
F, operate in soluble environments
17
Q
T/F Lipid Digestion is very minimal in the mouth and stomach
A
T
18
Q
Stomach contains __________ __________ where fat droplets are
A
gastric lipase
reduced in size
19
Q
the action of bile salts producing solubilized fat globules like micelles is known as the process
A
emulsification
20
Q
define emulsification
A
the breaking up of fat globules into smaller emulsion droplets
21
Q
list the amphiphilic molecules that are present in biles
A
bile salts and phospholipids
22
Q
Bile salts help solubilize …..
A
fat droplets into micelles
23
Q
fat globules produced by bile salts are targets for
A
lipases
24
Q
General characteristics of lipases
A
a class of esterases
hydrolyze glycerol backbones of lipids at specific locations of triacylglycerols (C1 or C3)
produced in the pancreas
25
define interfacial activation
phenomenon that describes rate enhancement of lipase when it contacts the lipid-water
interface.
26
Pancreatic Lipase is enhanced by a process known as
interfacial activation
27
interfacial activation process requires three molecules/proteins what are they ?
bile salts, mixed micelles of
phosphatidylcholine, and colipase
28
function of colipase
facilitates a hydrophobic platform that aids in binding lipid surfaces
29
T/F Lipase and colipase functions in a 2:1 ratio
F, they function on a 1:1 ratio
30
How does the presence of micelles affect lipase and colipase interactions in the active site
causes a change in the complex such that there is no longer access to the active site
31
Digestion of Lipids produces a mixture of
Fatty acids
mono- and diacylglycerols
32
mono- and diacylglycerols must be
absorbed by
mucosal cells in the small
intestines
33
what can be absorbed by mucosal cells and what can't?
Free monoglycerides
and fatty acids
NOT micelles
34
How do bile salts also aid in absorption ?
by better facilitating diffusion of lipids into mucosal cells
35
Intestinal fatty acid-binding protein interacts with
fatty acids forming a complex inside the intestinal cells, increasing solubility
36
Lipids are transported as lipoproteins to other tissues for
storage and catabolism
37
Once inside the mucosal cell, what happens to FAs
they are reesterfied into TAGs
38
what molecules are packaged together to form chylomicrons
TAGs, cholesterol esters, apoproteins,
and vitamins
39
name a transport protein in lipids that is part of the exogenous pathways
chylomicrons
40
Chylomicrons are transported via the
lymph system
41
List the Major Structural Components of Lipoproteins
1. Triacylglycerol
2. Phospholipid
3. Cholesterol
4. Apoprotein
42
what are the building blocks of proteins
amino acids
43
dietary proteins are digested into
tripeptides
dipeptides
amino acids
44
excess amino acids carbon skeletons can be salvaged for
GNG
FA biosynthesis
Ketone bodies biosynthesis
45
what are the three functions of Protein Degradation
1. to store nutrients for times of need in the form of proteins
2. to eliminate proteins that are harmful to the cell and could accumulate
3. to permit regulation of cellular metabolism
46
List 3 proteolytic enzymes
Chymotrypsin
Trypsin
elastase
Serine Protease
47
trypsin
cleaves R,K
48
Chymotrypsin
cleaves aromatic A.A W,Y
49
Serine Protease
contains catalytic triad
Asp, His, Ser
cleaves peptide bonds
50
where does digestion of proteins occur
stomach
51
proteins are cleaved by
porteolytic enzymes
52
elastase
cleaves non polar A.A
Gly,Ala
53
what is the function of storing nutrients for times of need in form of proteins important in
muscles
54
what can the elimination of proteins that are harmful to cells and accumulate cause
aggregation issues
mismanaged production of metabolites
55
what roles does permitting regulation of cellular metabolism via protein degradation have
controls level of enzymes directly
control levels of regulatory proteins that impact enzymatic activity
56
extracellular and intracellular proteins may be disgested by
lysosomal proteases
57
proteins can be degraded by
lysosomes
poly-ubiquitination
58
Proteasome function
unfolds proteins in an ATP-dependent process and degrades them
59
Lysosome characteristics
contain over 50 proteases
pH is 5
Nonspecific degradation of proteins
rapid degradation of proteins
60
T/F lysosomes are Single-membrane vesicles found in all eukaryotic cells
F, found in ALMOST all eukaryotic cells
61
what is the main function of lysosomes
degradation of incoming materials of all kinds like organelles proteins and lipids
62
what is the pH of lysosomes
4.5-5
63
why is it important for pH of lysosomes to be about 5
because its roles i degradation and having an acidic environment destabilizes protein folding making it an easier target for degradation
64
How do cargoes ( proteins) that need to be degraded by lysosomes get there?
endocytosis
autophagy
65
endocytosis for degradation of protein
comes from outside the cell crossing membrane to cytoplasm where lysosomes are
66
define autophagy for degradation of proteins and where it goes
comes from inside the cell itself, in the cytoplasm and goes to lysosome
67
how are products generated from lysosomal degradation released
diffuse out of the lysosome
actively transported to cytosol by lysosomal proteins for the re-use by the cell
68
define non essential amino acids
body can biosynthesize it within itself does not come from diet
69
define essential amino acids
A.A that only come from our diets
OR
the breaking down of proteins that are no longer needed that contain the essential amino acids
70
why is lysosomal protein degradation used in essential amino acids
helps us obtain amino acids that come from our diet
71
amino acids can be ....
glucogenic
ketogenic
both
72
carbon skeletons of glucogenic amino acids are degraded to
pyruvate
a-KG
succinyl CoA
fumarate
OAA
73
carbon skeletons of ketogenic amino acids are degraded to .... and what can they converted to
acetyl-CoA
fatty acids or Ketone Bodies
74
ubiquitination characteristics
a selective ATP-dependent ubiquitin mediated pathway
Specific protein degradation
covalent bond formed between target and ubiquitin
75
T/F ubiquitin is a small 76 residue protein found in ALL eukaryotic cells
T
76
c terminus of ubiquitin function
contains a carboxylate side chain that will form a covalent bond to tagged protein
77
Lysine residue function
attachment point for multiple ubiquitin
joining of lys residues form isopeptide bond
78
what is the tag that gets recognized by proteasome
poly-ubiquitin tag
79
T/F For proteins to be targeted by proteasome it needs a poly-ubiquitinated protein
T
80
name the 3 enzymes of ubiquitination
ubiquitin activating enzyme
ubiquitin carrier protein ( ubiquitin conjugating enzyme)
ubiquitin protein ligase
81
function of ubiquitin activating enzyme
utilizes ATP to form thioester bond with C-terminus of ubiquitin
82
function of ubiquitin carrier protein
transfer ubiquitin to a specific cys-thiol bond of E2 ( to maintain energy from thioester bond)
83
function of ubiquitin protein ligase
selects proteins for degradation
forms binding sites for each of 2 substrates
84
how does ubiquitin protein ligase form binding sites for 2 substrates
Binds E2-S-ubiquitin
transfer ubiquitin to lysine residues of target protein by breaking the thioester bond
will continue to go through cycle to get polyubiquitinated
85
function of Cap in proteasome
allows for the entry of poly-ubiquitinated protein into proteasome
86
what is the fate of ubiquitinated proteins
proteasomes
87
ubiquitin marks proteins for
proteasome degradation
88
which proteins get ubiquitinated?
N-terminal amino acid with shorter half lives
PEST sequence ( pro-glu-ser-thre)
regulated ubiquitination ( slide 17)
89
KFERQ- Motif is specific for what kind of degradation
lysosomal
90
lost from tissues that atrophy affects protein degradation how?
increases the rate of degradation
91
where can the KFERQ-Motif sequence be found
in cytosolic proteins as a target for lysosomal degradation under fasting conditions as part of autophagy
92
the KFERQ sequence is recognized by
chaperone mediated autophagy pathways
93
function of chaperone mediated autophagy in lysosomal degradation
is a recognition protein that will look for specific sequence to bring it to lysosome so that autophagy can occur
94
KFERQ meaning in terms of AA
K and R= up to 2 positively charged residues (R,K)
F = up to 2 hydrophobic residues ( I,F,L,V)
E = single negatively charged residue (E,D)
95
define transanimation
transfer of amino groups
moving it from one molecule to another
96
aspartate aminotransferase function in matrix
OAA makaes a-KG while Glutamate and a-KG make aspartate
97
aspartate amino transferase functino in intermembrane space
takes apartate and a-KG to regenerate glutamate and OAA
98
what molecule do transaminases use ( known as E)
PLP (pyridoxal-5-phosphate)
99
PLP is covalently attached to
enzyme lysyl residue via a Schiff's base
100
why is a schiff's base conjugate to the pyrimidine ring in transaminases
it is the center of activity
101
as an amine is transferred PLP becomes
pyridoxamine-5-phosphate (PMP)
102
transaminases are a class of enzymes that utilize what kind of mechanism
ping pong mechanism
103
purpose of ping pong mechanism in transaminases
to transfer amino groups from amino acids to for a-keto acids and new A.A
104
Transamination reactions occur in two stages what are they
conversion of an A.A to a-keto acid
Conversion of an a-keto acid to an A.A
105
T/F transamination is a key reaction of AA metabolism and requires PLP
T
106
increased concentrations of specific transaminases high in the blood are indicative of
Heart attack
Liver damage
107
how can the organs such as heat and liver show damage in amino acid metabolism
leak intracellular contents to the blood stream
108
where can glutamate DH be found
in the mitochondria
109
Glutamate DH in terms of usage of electron acceptors
only known enzyme that can use either NAD+ or NADP+ as electron acceptors
110
how does Glu DH remove NH4+
Oxidative deamination
111
T/F Glu DH has a low Km for Glu , meaning high affinity
F, it has a High Km therefore a low affinity for Glu
112
T/F Glu DH is a reversible enzyme
T
113
Glutamate DH is a regulatable enzyme, under what conditions will it be inhibited and when will it be activated
High energy , GTP and NADH inhibit
Low energy, ADP and NAD+ activates
114
what is the intermediate GDH undergoes in its mechanism
a-Iminoglutarate
115
Ammonia intoxication produces
a comatose state
116
T/F Ammonia is not toxic to animals
F, it is
117
high concentrations of ammonia shift equilibriums to
favor glutamine
118
Glutamate and its derivative GABA are NT, the shift in equilibrium does what
lowers the concentration of these NT
119
Draw the Urea Cycle, include name of enzymes , and structures
slide 37 of amino acid metabolism
120
In the liver, energy is produced in the form of glucose thus the formation of ____________ is favored, important for _________ __________ as ________
pyruvate
nitrogen removal
urea
121
Draw the cycle of using amino acid alanine in the muscle and liver ( Hint: similar to Cori Cycle)
slide 44 in amino acid metabolism
122
ornithine is also used in ___________ _____________ - involves nitrogen
polyamine biosynthesis
123
Inhibition of polyamine biosynthesis effects
stops/diminishes cell growth
making it an attractive drug target of fast acting cancers
124
What other 3 molecules can ornithine be converted to
Putrescine
Spermidine
Spermine
125
what is the mitochondrial enzyme that is usually the rate limiting step of Urea Cycle
Carbamoyl Phosphate Synthetase I
126
What activates the carbamoyl P synthetases I
high levels of N-acetyl Glutamate
high levels of amino acid glutamate
high levels of urea and ammonia
127
acetyl-CoA + Glu -->
N-acetyl glutamate
128
mutations which reduce efficiency of urea cycle can lead to
hyperammonemia
lethargy
mental retardation
129
how can mutation that reduce efficiency of urea cycle be treated
change in diet
adding NAG ( N-acetyl-glu) analogs
increasing arginine
130
what enzyme is involved:
2 ATP + HCO3- + NH3 --> carbamoyl P + 2 ADP + 2 Pi
carbamoyl P synthetase I
131
name the enzyme that is a 3 step reaction that is the rate-limiting step for urea formation
carbamoyl P synthetase I
132
Describe the three step reaction of carbamoyl P synthetase I
1. ATP is used to activated bicarbonate to form carboxyphosphate
2. Ammonia (NH3) attacks carboxyphosphate to form carbamate and inorganic phosphate
3. A second ATP serves as a phosphate donor to form carbamoyl-phosphate
133
ornithine transcarbamylase function
allows for the formation of citrulline by using carbamoyl phosphate and ornithine
134
what molecule that is part of the urea cycle gets exported from the matrix into cytosol
citrulline
135
What is the cost of argininosuccinate synthetase in the urea cycle
2 ATP
136
In the urea cycle , what serves as the source for the second nitrogen
Aspartate
137
describe the reaction of argininosuccinate synthetase in the urea cycle
Aspartate comes into play in this enzyme
AND
Citrulline is activated by ATP, and PPi is hydrolyzed to drive reaction
138
function of arginosuccinase in the urea cycle
removes the nitrogen from aspartate forming arginine and fumarate
139
what enzyme facilitates the formation of argininosuccinate
argininosuccinate synthetase
140
what amino acid is the precursor of urea
arginine
141
function of arginase
uses hydrolysis to form urea as a waste product and forms ornithine
(gets transported back to matrix to go through cycle again)
142
Arginine --> urea + ornithine
catalyzed by what enzyme
arginase
143
arginosuccinate --> Arg + fumarate
catalyzed by what enzyme
arginosuccinase
144
citrulline + Asp --> arginosuccinate
catalyzed by what enzyme
arginosuccinate synthetase
145
what are the fates of fumurate apart from the urea cycle
1. reenters mitochondria to malate-aspartate shuttle to promote TCA
2. converted to malate via fumarase to OAA cia malate DH ---> GNG
146
why is the formation of alanine and a-KG favored in the muscle
because amino acid biosynthesis allows for muscle repair
147
tyrosine is formed by
phenylalanine hydroxylase
148
Lipids are transported as lipoproteins to other tissues for
storage or catabolism
149
list the different types of lipoproteins based on their protein content ( low to highest)
chylomicrons
VLDL
IDL
LDL
HDL
150
chylomicrons are composed of
dietary TAGs, cholesterol, and cholesteryl esters
151
where are chylomicornos formed
in the intestinal mucosal cells after absorption
152
describe the exogenous pathway as it relates to chylomicrons
gets released to intestinal lymph for transport through lymphatic vessels to large veins for delivery throughout the body
153
what lipoproteins are synthesized by the liver to transport internally produced triacylglycerols and cholesterol from the liver to the tissues
VLDL , IDL, LDL
154
what lipoprotein transportscholesterol and other lipids to the liver from the
tissues
HDL
155
function of VLDL
transport TAGs and FAs from liver to tissues
156
where are VLDLs released
to the blood stream as part of the endogenous pathways
157
where is VLDL biosynthesized and what does it use
biosynthesized in the liver using cholesterol-rich chylomicron remnants and TAGs
158
what two lipoproteins are deliverers of triacylglycerol to cells in the body
Chylomicrons and VLDL
159
chylomicrons and VLDL have the same function how are they different?
Chylomicrons
- are formed in intestinal epithelial cells for transport
- dietary triacylglycerols are delivered to muscle cells and adipose tissue
- exogenous pathway
VLDL
- remnants of chylomicrons, as VLDL is biosynthesized in the liver
- part of endogenous pathway
- release to the blood stream
160
what lipoprotein is known as the transition particle between TAG transport and cholesterol transport
Intermediate density lipoprotein (IDL)
161
How is IDL formed
from the remnants of VLDL after removal of TAGs
162
how can HDL form more LDL
gets reabsorbed by liver
picking up cholesteryl esters from HDL
163
function of LDL
delivers cholesterol to cells where it is used in membranes ,
biosynthesis of bile salts in the liver, and
synthesis of steroid hormones
MAJOR cholesterol carrier in the blood stream
164
what lipoprotein is known as the major cholesterol carrier in the blood stream
low density lipoprotein
165
As VLDL is stipped of TAGs, they are remodeled in the liver to become ........
IDL and ultimately LDL , part of endogenous pathway
166
what are the major contributor of HDL
extra-hepatic cells
167
why are extra-hepatic cells the major contributors of HDL
cells cannot metabolize cholesterol
168
The HDL precursor is biosynthesized and secreted by
liver and small intestine
169
Lecithin- cholesterol
acyltransferase
an enzyme activated by
apolipoprotein A-1 that converts
cholesterol to cholesterol-esters
170
what is the only place where cholesterol can be
consumed for production of bile
acids
liver
171
what lipoprotein is involved in transport of cholesterol from the tissues to the liver – sometimes called reverse cholesterol transport
High density lipoprotein
172
Where is HDL biosynthesized and where is it released
in the liver and intestines for release in blood stream as a protein rich particle
173
Functions of HDL
used for cholesterol recovery ( cleans up excess cholesterol from blood for excretion)
delivers cholesterol to steroidogenic tissues ( adrenal glands, ovaries, testes)
174
define apoproteins and their functions
protein portion of lipoproteins ( coating surface) that dictate interactions
w/o lipid association
175
list the three examples of apoproteins
ApoA-1
ApoB-100
ApoE
176
Apolipoprotein A-1 (ApoA-1) binding occurs in ..... and what is their effect
chylomicrons and HDL
adds a high degree of hydrophilicity
177
what is known as a homotetramer producing a structure that can ideally wrap around and HDL particle
ApoA-1
178
Function of ApoAI
help clear fats and cholesterol from
white blood cells in arterial walls, helping ensure health of white blood cells.
179
ABCG1 transporter function
role in lipid homeostasis by controlling both tissue lipid levels and efflux of cellular cholesterol to HDL
180
ABCA1 transporter function
mediates efflux of cholesterol and phospholipids to lipid-poor apolipoproteins like ApoAI to form nacent HDL
181
how does ApoA1 intereact with HDL
it facilitates interactions with SR-B1 receptor within HDL at the liver
182
once ApoAI binds HDL to SR-BI and transfers its component lipids to the cell what occurs
Depleted HDL dissociates from the receptor and re enters circulation for scavenging cholesterol
183
LDL contains what kind of apolipoprotein
ApoB-100
in a ratio 1:1
184
what is LDL major role
major cholesterol carrier in the blood stream
185
function of ApoB-100
plays a role in LDL-receptor-mediated endocytosis
covers half the surface of LDL
186
LDL-receptors that target ApoB-100 are
transmembrane glycoproteins
187
the LDL-receptors specifically target ApoB-100 in
clathrin-coated pits that produce a clathrin-coated vesicle for endocytosis
188
ApoB-100 and cholesteryl-esters are hydrolyzed producing
amino acids , fatty acids, and cholesterol
189
Apolipoprotein E binds to
VLDL and chylomicrons
190
As VLDL is converted to LDL via IDL, what can remain bound to IDL
ApoE
191
Function ApoE
- enhance binding to LDL-receptors in liver and CNS
- facilitate the transfer of cholesterol to neurons in CNS
192
defects in ApoE4 have been correlated/linked to
increased chances of developing Alzeihmer's
193
stored fats are mobilized for
energy production (in animals)
194
activity of the enzyme hormone-sensitive triacylglycerol lipase is regulated by
high glucagon and epiniphrine levels
195
function of albumin
aids in transport of the predominantly hydrophobic FA coming from free FA and glycerol entering the bloodstream
196
High glucagon and epinephrine levels activate
cAMP dependent protein kinase A
197
once levels of cAMP are increased what occurs in terms of lipid metabolism
lipid droplets are more accessible to hormone-sensitive lipase
198
the rate of HSL hydrolysis dictates
rate of diffusion of FA passing across the adipocyte membrane to bloodstream
199
FA transported in blood via
serum albumin and enters muscle cells via FA transporter
200
FA are catabolized in
mitochondria
201
CD36 function
directly related to influx of FAs into the cell , they recognize FA chains
202
carnitine carries _______ _______ into the ___________ for ________
Fatty acids
mitochondria
oxidation
203
carnitine acyl-transferase I is inhibited by
High levels malonyl-CoA used for FA synthesis
204
once in the cytosol of muscle cells, FAs
must be activated and requires 2ATP investment for activation
205
Fatty acids in the cytosol of the cell must be activated by the attachment of
Coenzyme A
206
The priming reaction, or addition of CoA,in B ox is catalyzed by
acyl-CoA synthetases
207
function of acyl-CoA syntheetase
condenses FAs wtih CoA with simultaneous hydrolysis of ATP to AMP and PPi
208
T/F Formation of CoA ester is inexpensive energetically
F, it is expensive energetically
209
why does the activation of FA require the investment of 2 ATP
reaction barely break with 1 ATP hydrolysis
BUT
subsequent hydrolysis of PPi drives rxn forward
210
what enzyme has acyl-adenylate intermediate in its mechanism
Acyl CoA Synthetase
211
draw acyl-coA synthetase mechanism
slide 35 and 37 of lipid metabolism
212
activated acyl -CoA occurs in the _____________, but the process of fatty acid oxidation within the __________
cytosol
mitochondria
213
carrier carnitine function
accepts the acyl portion of activated FA through a transesterification reaction
214
what catalyzes the transesterification reaction in carnitine transport
carnitine palmitoyl transferase
occurs in outer mitochondrial membrane
215
what is released after the reaction carnitine palmitoyl transferase I
releases CoA in cytosol for use in more activation reactions
216
products from B-ox feed into
citric acid cycle
ETC/Oxidative Phosphorylation
217
define B-oxidation
the process of FA degradation in 2C units through an oxidative process involving the B-carboxyl group
218
Define Ketone bodies
special source of fuel and energy for ceratin tissues
219
some of the acetyl-CoA produced by FA ox in liver mitochondria is converted to
acetone
acetoacetate
b-hydroxybutyrate
( aka ketone bodies)
220
Ketone bodies are cource of fuel for
brain - during starvation
heart - fat burning mode
muscle
221
T/F ketone bodies are transportable forms of acetyl-CoA
T
222
why are ketone bodies useful as a special energy source
they are transportable forms of acetyl-CoA
223
Location of Ketogenesis
occurs in the liver mitochondria
224
first step in ketone body biosynthesis used what enzyme and where have we seen this before
thiolase (acetyl-CoA acetyltransferase)
reverse of last step in B-ox
225
what is a key intermediate in both ketone body and cholesterol biosynthesis
HMG-CoA
(hydroxymethylglutaryl-CoA)
226
what enzyme is the first committed step in the ketone body biosynthesis
HMG-CoA lyase
227
function of thiolase in ketogenesis
combines 3 acetyl CoA molecules allowing for release and production of energy in the form of CoA
228
what are the final two products made for HMG-CoA lyase
acetoacetate and acetyl CoA
229
Draw B-Hydroxy-B-methylglutaryl-CoA
Slide 5 of KB
230
where are acetoacetate and acetyl CoA released
acetyl CoA remains in the liver
acetoacetate gets released in the bloodstream
231
what are the fates of acetoacetate
gets converted to B-hydroxybuterate
can get converted to acetone
232
how does acetoacetate convert to B-hydroxybutyrate
redox reaction catalyzed by B-hydroxybutyrate DH
233
how does acetoacetate convert to acetone
undergoes a non-enzymatic decarboxylation since it is a B-keto acid
234
what dictates the fates of acetoacetate
based on the ratio of NADH/NAD
235
T/F the conversion to acetoacetate and D-B-Hydroxybutyrate is irreversible
F, it is reversible
236
during pro-longed periods of fasting, where glucose is limiting, the energy source of the body becomes? what pathway will kick in
breakdown of products of fats and thus KB
GNG will kick in to meet brains demands
237
T/F Ketone bodies are used for energy
T
238
KB are transported from the liver to other tissues in the bloodstream where _____________ and ___________________ can be converted to _______________ to produce energy
Acetoacetate
B-hydroxybutyrate
Acetyl CoA
239
when does the brain use ketone bodies
starvation
240
the heart gets much of its energy from
KB but also uses alot of FAs
241
why do we use KB for energy and not FA
KB are fast acting source for energy because of its quicker conversion to acetyl CoA , FA takes longer
242
fates of acetone
incorporated into lipid and skeleton structures
get excreted out as urine
gets exhaled
243
if NADH levels are higher than NAD+ what does this tell us in terms of BHB and acetone
B-hydroxybutyrate will be higher
244
fates of B-hydroxybutyrate
excreted as urine
used in metabolism by oxidative phosphorylation
245
function of B-hydroxybutyrate DH
takes any B-HB that has been generate and converts it it AcAc
uses NAD+ forming NADH as the electron acceptor
246
3-ketoacyl-CoA transferase function
uses succinyl CoA as a substrate producing acetoacetyl CoA and succinate
247
how are ketone bodies brought into the cell
monocarboxylate transporters
248
where does ketolysis occur
happens in other cells and NOT in the liver
249
liver lacks what enzyme thats important for ketolysis
3-ketoacyl CoA Transferase
250
why is it important for the liver to lack 3-ketoacyl CoA Transferase
liver is able to make its own energy and utilize other sources through B-Ox
so we want out other cells to have acces to KB for energy
251
what enzyme ensure that ketolysis will occur in target cells
3-ketoacyl CoA Transferase
252
define ketosis
accumulation of excess ketone bodies
253
define ketoacidosis
even larger amount of ketone bodies accumulate lowering the bodies pH to acidic levels
254
define diabetic ketoacidosis
associated with diabetic who cant use glucose in high amounts to keep up with energy demands , increasing the KB and acidic levels in blood stream
255
alcholic ketoacidosis
messe with the NADH/NAD+ polls
256
alcohol characteristics in ketoacidosis
diminishes hepatic GNG
decreases insulin secretion
increases lipolysis
impaired FA ox and ketogenesis
257
define nutritional ketosis
a diet high in fat and protein but low in carbs ( below 20g)
258
In nutritional ketosis it relies on what for glucose in the brain ? what about peripheral tissues
liver to keep up with glucose for the brain
fats and KB are supplied to peripheral tissues
259
if glucagon and cAMP levels are high and insulin levels are low what is occuring in nutritional ketosis
enhances glycogen breakdown and GNG activation
decreases lipid synthesis
260
what can a ketogenic diet that's used as part of dietary therapy helpful in treating
epilepsy
migraines
dementia
autism
261
define anaerobic exercise and what is its primary fuel
shorter bursts of energy such as weight training/high intensity interval training
carbs are used as the primary fuel
262
define aerobic exercise and what is its primary fuel
cardio excercise , low intensity and steady state for fat burning
relies on Fats
263
what causes a decrease in blood pH in ketoacidosis
increased concentration of acetoacetate and D-B-hydroxybutyrate in ionized form
264
cholesterols are precursors of
bile
steroid hormones
atherosclerotic plaques
265
cholesterol has structural and metabolic roles what are they
modulates membrane fluidity
serves as precursors for many molecules
266
atherosclerotic plaques are cause by _________ & what are the potential side effects
aggregation
heart attack and stroke
267
why is cholesterol prone to aggregation
it has a high degree of hydrophobicity
268
be able to recognize cholesterol
slide 2 on cholesterol powerpoint
269
Where can the only hydrophilic region of cholesterol be found
A ring of cholesterol
270
what makes cholesterol rigid
4 fused rings
271
what makes cholesterol weakly amphilic
lone hydroxyl group in A ring
272
cholesterol is synthesized from __________ ______ that comes from ________________
acetyl CoA
isoprene units
273
define isoprene units
5 C skeletons
274
fates of isoprene units
1. cholesterol
2. Fat Soluble Vitamins; Ubiquinone;hormones;carotenoids
275
how does cholesterol maintain fluidity of membranes
helps maintain order at high temps
helps offer a better barrier at low temps
276
how does cholesterol maintain order at high temps
offers rigidity for increased movement of FA tails
277
how does cholesterol offer a better barrier at low temps
increases interactions when movement stops at lower temps
phase change from fluid to gel-like solid
278
first step in cholesterol synthesis is the same as ketone body synthe except that it occurs in
cytoplasm
279
the second step in cholesterol is also same as KB , what occurs in this step in terms of cholesterol synthesis
uses HMG-CoA synthetase and attaches 2 C unit form acetyl Coa and forms HMG-CoA
280
draw HMG-CoA Synthase mechanism
slide 10 form cholesterol
281
what is the first committed step toward isoprene unit synthesis
HMG-CoA reductase
282
function of HMG-CoA reductase( cholesterol)
uses 2 NADPH to form mevalonate , resulting in a loss of CoA
283
Look at the mechanisms for HMG-Reductase I and II
slide 13 and 14 of cholesterol
284
List 6 characteristic of Cholesterol Biosynthesis
1. occurs in the liver
2. begins in the cytosol with synthesis of mevalonate from acetyl Coa
3. First step is a thiolase rxn
4. second step makes HMG-CoA
5. Third step - HMG-CoA reductase
6. HMG-CoA reductase is site of action of cholesterol
slide 16 on cholesterol ppt
285
define statin inhibitors of HMG-reductase
effective inhibitors that mimic the transition state
286
what enzyme is the principal site of regulation in cholesterol synthesis
HMG-CoA Reductase
287
How is HMG-CoA reductase regulated
1. Phosphorylation by cAMP (low energy status)
2. degradation via ubiquitin
3. gene expression
288
how does phosphorylation by cAMP affect HMG-CoA reductase
inhibits reductase therefore stopping biosynthesis pathway
289
if we have high levels of cholesterol how does this effect HMG-CoA Reductase
degrades HMG-CoA stopping biosynthesis
290
if we have high levels of gene expression how does this affect HMG-CoA
activates cholesterol biosynthesis , activates reductase
291
function of mevalonate-5-phosphotransferase
utilizes ATP as a phosphate donor to attach it to mevalonate to form phosphomevalonate
292
what enzyme of cholesterol synthesis begins the process of adding PPi tail
mevalonate-5-phosphotransferase
293
Thiolase utilizes an _______________ mechanism to allow for activation of nucleophilic attacks
with the reaction driven by the release of _________ ( cholesterol biosynthesis)
acid-base
CoA
294
function of phosphomevalonate kinase in cholesterol biosynthesis
adds a second phosphate using ATP as a donor forming 5-pyrophosphomevalonate
295
what enzyme in cholesterol biosynthesis completes the synthesis of PPi tail ( high energy leaving group)
phosphomevalonate Kinase
296
function of pyrophosphate mevalonate decarboxylase
forms isoprene unit using energy from decarboxylation and couple it with ATP
297
how does ATP fit into the reaction catalyzed by pyrophosphomevalonate decarboxylase
as decarboxylation occurs we leave behind e- and OH group has to leave so it occurs via ATP
w/o ATP it wouldn't be enough to hydrolyze P bond
298
product form from pyrophosphomevalonate decarboxylase
isopentenyl pyrophosphate
298
isopentenyl pyrophosphate is isomerized to produce dimethylallyl
pyrophosphate via what enzyme
isopentenyl pyrophosphate isomerase
298
T/F hydrolysis of ATP drive long chain of otherwise unfavorable e- transfers in third step cholesterol biosynthesis
F, it is the fourth step
299
what are the two isoprene units forms in cholesterol biosynthesis
isopentenyl pyrophosphate
dimethylallyl pyrophosphate
300
function of isopentenyl pyrophosphate isomerase
allows for the two isoprene units to be easily interconverted
301
what allows for the 5C units to easily form long chains/ condense
via cleavage and hydrolysis of PPI
302
function of prenyltransferase, product formed ( give number of C) , and direction of reaction
combines 2 5C units by releasing PPi
to form geranyl pyrophosphate (10C)
moves in head to tail direction
303
what can prenyltransferase also do other than condensing a 5C units to forming a 10 C unit
releases another PPi
AND
combines geranyl pyrophosphosphate (10C) and isopentyl pyrophosphate (5C) to produce farnesyl-pyrophosphate ( 15C)
head to tail
304
head to head condensation to form squalene with the use of NADPH is catalyzed by what enzyme
squalene synthase
305
function of squalene synthetase
NADPH dependent enzyme, that catalyzes the condensation of two farnesyl pyrophosphates
to produce squalene
306
squalene from mevalonate is driven by
ATP hydrolysis, decarboxylation and PPi hydrolysis
307
condensation of 3 mevalonate forms
farnesyl PPi
308
two farnesyl PPi link to form
squalene
309
function of squalene epoxidase
catalyzes addition of an epoxide ring forming 2-3 oxidosqualene
310
cleavage of epoxide ring leads to
cascade of e- movement that conversts polyisoprene into lanosterol
311
squalene monooxygenase converts
squalene to squalene-2,3-epoxide
312
a ____________ converts the epoxide to lanosterol
cyclase
313
the conversion of squalene to epoxide occurs in
the ER membrane
314
acyl Coa cholesterol transferase
transfers acyl CoA moeitey to cholesterol at C3 and forms and ester bond
315
cholesterol is exported form liver as
VLDL
316
ApoC-II activates
extracellular lipoprotein lipase in capillaries and unloads TAG
317
TAG are unloaded via
ApoC-II and Lipoprotein
318
regular, vigorous exercises raises ______ and a low fat diet that avoids red meat reduces __________ ___________ __________
HDLs
serum cholesterol levels
319
ApoB-100 binds _______ ____________ and delivers ______________ to peripheral tissue
LDL receptors
cholesterol
320
in response to the bodies response to high cholesterol levels , when decreased HMG-CoA reductase causes
decrease mRNA levels
increase enzyme degradation
both of these will decrease cholesterol synthesis
321
in response to high cholesterol levels, there is a decreased LDL receptors which causes
reduces uptake of cholesterol in the blood
322
In response to high cholesterol levels, when some cholesterol is shipped back to liver via HDL how is this done
activates ABCA1 transport protein which binds cholesterol inside the cell and passes it out to blood stream in form of HLDL
in liver some cholesterol is turned to bile transported to the intestine
323
what is the bodies response when there is high cholesterol levels
decrease in cholesterol biosynthesis
decrease in HDL levels
decrease in bile salts
decrease in absorption
decrease in LDL receptors
increase in VLDL receptors
324
what happens to cholesterol in excess VLDL and LDL
some deposited on walls of blood vessels forming plaque
atherosclerosis
325
define familial hypercholesterolemia FH
genetic lack of LDL receptors
326
define tangier disease
lack of ABCA1 transporter
causing a decrease in HDL receptors
327
The consequence of the loss of LDL
receptors is two-fold:
levels of LDL (and VLDL) rise in the blood stream and
(2) the uptake of LDL in
extrahepatic cells decreases, leading to a decrease in HDL
328
Diminished levels of HDL coupled with increased levels of
VLDL/LDL lead to a buildup of cholesterol that leads to
a buildup of cholesterols that lead to pro-inflammatory response, leading to calcification of plaques in arteries and blood vessel damage
329
many drugs that lower serum cholesterol are
mevalonate analogs that inhibit HMG-CoA reductase
330
tricarboxylate transport system function
transfers acetyl-CoA in form of citrate into the cytosol for fatty acid synthesis
331
FA synthesis begins with
carboxylation of acetyl-CoA to generate malonyl-CoA
332
fatty acid synthase enzyme function
carries out seven reactions and lengthens a fatty acid two carbons at a time
333
function of elongases
add extra carbons to the FA
334
function of desaturases
allows for DBs to form
335
TAGs are synthesized from
from glycerol and fatty acids
336
what is the major way that acetyl CoA gets transported out of the cell in the form
of citrate
337
how is citrate formed
combining acetyl CoA with OAA in TCA via citrate synthase
338
how does pyruvate get converted to OAA
anaplerutic reaction using pyruvate carboxylase
339
what is the major source of cytosolic acetyl CoA
Citrate via ATP citrate lyase
340
what serves as the building blocks for malonyl-CoA
Acetyl CoA
341
Acetyl-CoA is generated in the mitochondrion by either
pyruvate dehydrogenase complex or beta oxidation
342
ATP-citrate lyase function
catalyzes the
conversion of citrate to oxaloacetate and acetyl-CoA in the cytosol
343
what is going to happen when our energy levels are high
decrease in TCA
AND
increase in citrate
344
draw the tricarboxylate transport system
slide 6 on FA biosynthesis
345
to synthesize lipids must export
acetyl CoA to cytoplasm via citrate
346
why not stop OAA conversion at malate in the cytosol
we want increase in NADPH level for reductive biosynthesis
347
acetate units need for FA biosynthesis are activated by
the formation of Malonyl-CoA at the expense of ATP
348
driving force of the condensation reaction is the ........... in FA biosynthesis
exergonic decarboxylation of Malonyl CoA
349
chain elongation stops at
palmitoyl CoA
350
what enzyme commits acetate to FA synthesis
acetyl-CoA carboxylase
351
what must occur first to be committed step in FA biosynthesis
carboxylation of acetyl CoA to form malonyl CoA
352
what are the three enzymes of ACC
biotin carboxyl carrier
biotin carboxylase
transcarboxylase
353
what enzyme utilizes biotin and ATP to activate CO2 for carboxylation of acetyl-CoA
acetyl CoA carboxylase
354
draw the acetyl coA carboxylase mechanism
slide 11 FA biosynthesis
355
protomers
inactive/inhibit
T state in ACC
356
polymers
multiple protomers together
R state ( active )
357
what is positive allosteric ACC enzyme
Citrate
358
what is the negative allosteric ACC enzyme
Palmitoyl CoA
359
what are the effects of citrate on ACC
it activates it
favors R state and therefore favors polymer formation
360
what are the effects of Palmitoyl CoA on ACC
inhibits ACC
stabilized T state therefore in favors protamers
361
ACC hormonal control involves
phosphorylation of Ser79
362
hormonal control of ACC is catalyzed by
AMP-dependent protein Kinase that is part of cAMP independent pathway
363
AMPK effec on ACC
leads to inactivation of ACC
364
when levels of glucagon and epinephrine are high how does this affect ACC
activates protein kinase A which phosphorylates ACC leading to inhibition
365
T/F ACC can exist in different isoforms based on tissue specificity
T
366
Adipose tissue contains what kind of ACC isoform
cytosolic ACC1 where FA biosyn occurs
367
tissues that lack FA biosyn have much higher ratios of
ACC2
368
Function of ACC2
produces malonyl CoA as a way to inhibit the carnitine transporter so FA cant enter matrix for B ox and differe stop FA biosynthesis
369
why does the liver have both ACC1 and ACC2 forms
relies on its own ability to do its own FA biosynthesis and relies on FATS for energy source
370
define nonalcoholic fatty liver disease
hepatic accumulation of excess triglycerides
371
what is the leading cause of morbidity and mortalinty in atients with NAFLD
cardiovascular disease
372
effects of high insulin levels on ACC
activates ACC
Increasing FA biosynthesis
Increase energy
373
Compare and contrast B-ox and FA biosynthesis
B-Ox:
- occurs in matrix
- tagged by CoA as carrier group
- e- flow through ox. of carbon compounds to produce e- carriers NADH and FADH2
- in the l configuration
- Acetyl CoA used as C2 unit
FA:
- occurs in cytoplasm
- tagged by ACP as carrier group
- go through reduction reactions to form FAs and use NADPH
- in D configuration
- uses malonyl CoA as C2 unit
374
what is the condensing enzyme of FA biosynthesis
B-ketoacyl-ACP synthase
375
high levels of fatty acyl-
CoAs serve
feedback inhibitors for FA metabolism
376
Acetyl Transacylase function
takes acyl portion of acetyl CoA and transfers to acyl
carrier protein (ACP), releasing CoA
377
Malonyl Transacylase function
malonyl portion of malonyl CoA is
transferred to ACP, release CoA
378
what enzymes are required to produce the substrates for β-ketoacyl-ACP synthase
Acetyl Transacylase
Malonyl Transacylase
379
β-ketoacyl-ACP synthase function
serves to condense malonyl-ACP
and acetyl-ACP,forms acetoacetyl-ACP
380
how does B-ketoacyl-ACP synthase condense malonyl ACP and acetyl ACP
via decarboxylation occurs allowing for the formation of the
4-carbon unit acetoacetyl bound to ACP
381
β-Ketoacyl ACP reductase function
uses NADPH to reduce a ketone
producing a hydroxyl group in
formation of β-hydroxybutyryl-
ACP
382
3-Hydroxyacyl-ACP dehydratase function
removes water in a dehydration
reaction, forming a double bond in
the product α,β-trans-butenoyl-
ACP
383
Enoyl ACP-reductase function
reduces the
double bond using NADPH to form
butyryl-ACP
384
what is the final step of FA biosynthesis after the 7 reactions
palmitoyl thioesterase (TE)
385
function palmitoyl thioesterase
allows for the release from acyl carrier protein sulfhydryl group so that palmitate gets released
386
elongation beyond 16 C occurs in
in ER and mitochondria
387
what is the substrate for elongation beyond 16 C
acyl CoA
388
T/F all natural double bonds in FA are cis
T
389
fatty acid synthase contains how many active sites
six active sites for seven reactions
390
what is the key intermediate for synthesis of TAG and other complex lipids
phosphatidic acid
391
what are the enzymes required to take dihydroxyacetone phosphate to phosphatidic acid
glycerol-3-phosphate DH
glycerol-3-phosphate acyltransferase
1-acylglycerol-3-phosphate acyltransferase
392
what are the precursor of glycerophospholipid and what is the function of glycerophospholipid
1,2-diacylglycerol phosphatidic acid
lipid in membranes
393
what are the precursor of spingolipid-sphingomyelins and its function
1,2-diacylglycerol phosphatidic acid
lipid in membranes
394
what is the precursor of sphingoglycolipids ( cerebrosides and gangliosides) and their functoin
palmitoyl-CoA serine
lipids in membrane
395
what lipid gets metabolized from arachidonic acid
prostaglandins
396
what is the precursor of prostaglandins and function
C20 FA - arachidonate
inflammation
397
PLA2 releases arachidonic acid is precursor of
eicosanoids
398
T/F eicosanoids are local hormones
T
399
tissue injury and inflammaation triggers
release of arachidonate and eicosanoid synthesis
400
T/F eicosanoids are precursors of arachidonic acid
T
401
characteristics of eicosanoids
exert effects a very low concentrations
have very short half lifes
act at sites near their biosynthesis
synthesized from arachidonic acid in ER
402
release of eicosanoids is stimulated by
histaines , hormones, and proteases
403
eicosanoids are also produced when
tissues are injured producing inflammation and pain
404
thromboxane A2 is produced by
platelets to stimulated platelet aggregation
405
COX2 is produced in high levels in rensponse
to pain
406
coxibs become important for
treatment of inflammatory diseases like arthritis
407
what is the activated form of FA
fatty acyl CoA
408
where is abnormal adrenoleukodystrophy protein found
peroxisome
409
function of ALD protein
responsible for breaking down very long chain FAs
410
the accumulation of very long FAs damages
myelin sheath results in neurological problems
encoded by ABCD1 gene
411
function of peroxisomes
takes really long FAs and helps break them down as a way to help and speed up function of mitochondria
412
glyoxysomes
metod of FA b-ox in plans
413
what are the three enzymes used in B-oxidation in peroxisomes
acyl-CoA oxidase, peroxisomal enoyl-CoA hydratase, peroxisomal thiolase
414
Acyl-CoA oxidase catalyzes a reaction using
fatty acyl-CoA and molecular oxygen to produce trans-Δ2-enoyl-CoA
and
hydrogen peroxide via a FAD-cofactor, where electrons are transferred directly to O 2
producing H2O2
415
FA oxidation in peroxisomes difference than B-ox
produce 1.5 fewer ATP per 2-C units
enzyme catalse is present to address the generation of H2O2
416
how is peroxisomal thiolase different than thiolase in b-ox
has specificity for longer FA chains and does not recognize substrates with 8C or less
417
how does transport occur in peroxisome
via ALD protein
418
in perozisomes what breaks down hydrogen peroxide to H2O and O2
catalase
419
what is the first enzyme in peroxisomal FA oxidation
acyl-CoA oxidase
420
describe the process that Fatty Acyl CoA undergoes through in B-Ox
proceeds through oxidation in which 2 C units are removed producing acetyl CoA and remainder of fatty acyl CoA molecule until all possible 2 Carbon units have been converted to acetyl-CoA
421
where does B-Ox occur
in the mitochondri a
422
what enzyme that is the first step of B-ox that forms a trans-double bond
acyl-CoA DH
423
acyl CoA DH converts fatty acyl CoA to
trans-Δ2-enoyl-CoA
424
mitochondria has 4 different acyl-CoA DH how do they differ
they differ based on their specificity b/c FA can occur in a # if diff length
425
majority of SIDS occur b/c
long-chain FA oxidation effects
426
the mechanism of acyl CoA DH involves
proton abstraction
double bond formation
hydride removal by FAD
427
function of enoyl CoA hydratse
splits H2O across dbl bond
forms 3-L -hydoxyacyl-CoA
428
what enzyme converts trans - Δ2 - enoyl- CoA to 3-L-hydroxyacyl-CoA
enoyl-CoA hydratase
429
what is the second enzyme used in B-Ox that is similar to fumarase
enoyl-CoA hydratase
430
function of 3-L-hydroxyacyl-CoA DH
NAD+ dependent dehydrogenation
converts 3-L hydroxyacyl-CoA to B-ketoacyl-CoA
431
addition of CoA, is catalyzed by a family of enzymes called _________ _________ and can be found in ....
acyl-CoA synthetases
endoplasmic reticulum or outer mitochondrial membrane
432
Fatty acids pass through the outer
mitochondrial membrane using
carnitine
palmitoyl acyltransferse I
433
The translocation of acyl-carnitine across the inner mitochondrial membrane is mediated by
carnitine
carrier protein
434
Upon entry into the matrix, the acyl portion is transferred to CoA using as transesterification reaction catalyzed by
carnitine palmitoyl transferase II
435
function of B-ketoacyl CoA thiolase
cleaves B-ketoacyl with a thiol group of CoA
converts B-ketoacyl CoA to acetyl coA and remaining acyl CoA is 2C shorter
436
draw B-Ox of palmitic acid
slide 16 on B-Ox slides
437
equation used to calc number of rounds of B-ox
(C/2)-1
438
equation used to calc number of acetyl CoA
C/2
439
Each round of B-Ox Yields
1 NADH
1 FADH2
1 acetyl-CoA
440
Each acetyl CoA enters TCA and yiels
1 FADH2
1 GTP
3 NADH
441
The process of activation of FA comes in the cost of
2 ATP
442
most FAs have Cis db what is the problem with this for B-ox
b-ox uses trans double bonds
cis db is not a substrate for the 4 enzymes involved in B-ox
443
what is the solution to monounsaturated FAs when a cis DB is encounteres
use of enoyl-CoA isomerase
444
function of enoyl CoA isomerase
catalyzes isomerizaation reaction
converts cis- Δ3 double bond to trans- Δ2 double bond
445
list the 3 issues that can arise in the B-ox of Polyunsaturated FAs
presence of beta,gamma DB ( need a,B for enoyl CoA hydratase)
presence of Δ4 double bond inhibits enoyl-CoA hydratase
the Δ3 double bond product
is not a substrate for
enzymes in β-oxidation
446
how is the presence of beta,gamma DB resolved in polyunsat FAs
enoyl CoA isomerase moves location of DB from Cis-3 to trans-2
447
how is the presence of Δ4 double bond inhibits enoyl-CoA hydratase resolved
use of NADPH dependent enzyme 2,4-dienoyl-CoA reductase
in mammals requires 3,2-enoyl-CoA isomerase
448
function 2,4-dienoyl-CoA reductase
reduces Δ4 DB to 3,4 trans DB
449
function of 3,2 enoylCoA isomerase
flips location of trans DB to C2 and C3
450
how is the Δ3 double bond product
that is not a substrate for
enzymes in β-oxidation resolved
3,5-2,4 dienoyl CoA isomerase
451
3,5-2,4 dienoyl CoA isomerase function
converts the trans delta 3 DB to a trans delta 2 DB so that it becomes a substrate for 2,4-dienoyl CoA reducatase
452
function of acyl CoA DH
creates a trans DB between C2 and C3 of fatty acyl CoA
453
enoyl coA hydratase adds water to create trans DB what happens to OH
transferred to C3
454
function of 3-L hydroxylacyl CoA DH
oxidizes OH to a ketone using NAD+
455
what is the fate of 3C unit propionyl CoA from odd # B-ox of FA
converts to succinyl CoA
456
what are the 3 enzymes involved that converts propionyl CoA to succinyl CoA
propionyl CoA carboxylase
methylmalonyl CoA racemase
methylmalonyl CoA mutase
457
what is the cost of a cis DB
1 FADH2
458
what is the cost of the presence of a Delta 4 DB
1 NADPH but gets repayed later by NADH
cost = 2.5 ATP
459
how do we use propionyl CoA as energy
produces malate via 3 enzymes ( succinyl CoA synthetase, succinate DH, fumarase)
transported to matrix via malate asp shuttle
malic enzyme converts it to pyruvate
converted to acetyl CoA via PDHC
fuels TCA cycle
460
proline is made from
glutamate
461
function of THF
interconverts several one carbon copmds or fragments
462
in bacteria aspartate biosynthesizes
Lysin
methionine
threonine
463
leucine isoleucine and valine are derived from
pyruvate requires TPP enzyme
464
what amino acids are synthesized from glucose derivative
Phe
Tryptophan
Tyr
465
histidine involves
5-phosphoribosyl-a-pyrophosphate used in nucleotide biosynthesis
466
Apolipoproteins are lipid binding proteins that aid in
the transport of triacylglycerols.
467
apolipoproteins protein moieties are recognized by
receptors on cells surfaces of
muscle and fat cells.
