Metabolism Review Dr. Tuohy Flashcards
(99 cards)
1
Q
glucose synthesis and glucose degradation occur in the
A
cytosol = glycolysis and gluconeogenesis
2
Q
fatty acid synthesis occurs in the
A
cytosol
3
Q
the 3 pathways that occur in the cytosol are
A
glucose and fatty acid synthesis, and glycolysis
4
Q
Oxidative phosphorylation occurs in the
A
mitochondria
5
Q
fatty acid degradation (beta oxidation) occurs in the
A
mitochondria
6
Q
TCA cycle occurs in the
A
mitochondria
7
Q
3 things that happen in the mitochondria
A
TCA cycle
fatty acid degradation
Oxidative phosphorylation
8
Q
allosteric modification is covalent or non covalent?
A
non covalent
9
Q
covalent modification of enzymes are fast/slow processes
A
slow
10
Q
speed of a reaction depends on
A
the amount of activation energy
11
Q
Most enzyme-catalyzed reactions proceed from ___times faster than uncatalyzed reactions.
A
(10)^3 - 10^8 x faster
12
Q
enzymes affected by
A
temperature pH and cofactors
13
Q
Holoenzyme is an Enzyme with its
A
cofactor
14
Q
Apoenzyme is the __ portion of the haloenzyme
A
protein
15
Q
__is a tightly bound coenzyme that does not dissociate
A
prosthetic group
16
Q
pyruvate dehydrogenase coenzyme is
A
thiamine pyrophosphate
17
Q
monoamine oxidase coenzyme
A
flavin adenine nucleotide
18
Q
lactate dehydrogenase coenzyme
A
nicotinamide adenine dinucleotide (NAD)
19
Q
glycogen phosphorylase coenzyme
A
pyridoxal phosphate
20
Q
acetyl coA carboxylase coenzyme
A
coenzyme A (coA)
21
Q
pyruvate carboxylase coenzyme
A
Biotin
22
Q
methylmalonyl mutase coenzyme
A
5’-Deoxyadenosyl cobalamin
23
Q
thymidylate synthase coenzyme
A
tetra hydrofolate
24
Q
carbonic anhydrase coenzyme
A
Zn2+
25
carboxypeptidase coenzyme
Zn2+
26
EcoRV coenzyme
Mg2+
27
Hexokinase coenzyme
Mg2+
28
Urease coenzyme
Ni2+
29
1. cofactors are not proteins
| 2. if the cofactor is organic, it is called more specifically a
1. not
| 2. coenzyme
30
in michaelis-menten kinetics what are the y and x axis
```
y = initial velocity
x = substrate concentration
```
31
in michaelis-menten kinetics the curve is what shape
hyperbolic shape
32
in michaelis-menten kinetics, how do you find Km
you find 1/2 Vmax and then go down to x axis
33
the top of the curve in michaelis-menten kinetics is the
Vmax
34
in the hyperbolic shape, the initial reaction velocity is first/zero order?
first order
35
in the hyperbolic shape, as we approach Vmax the reaction becomes _ order
zero order
36
if you increase the enzyme concentration in the reaction what will change? Vmax/Km
Vmax will change but not the Km
37
the rate of reaction is directly proportional to the enzyme/substrate concentration?
enzyme concentration at any substrate concentration
38
if enzyme concentration is halved then the initial velocity will be
also halved
39
covalent modification of enzymes vs allosteric modification of enzymes. Reversible inhibitors bind enzymes through _ bonds
non covalent
40
the 2 most common inhibition
competitive and non competitive
41
methotrexate used in cancer therapy is an example of what kind of inhibition
competitive. binds dihydrofolate reductase that is the enzyme needed to make tetrahydrofolate (THF). when it binds it wont the appropriate substrate in, so we don't make THF, so the cell cant make nucleotides, so the cell dies. Kills the cancer cells.
42
what are the axis of the lineweaver burk plot?
1/V is the y
| 1/[S] is x
43
lineweaver burk plot is a __ plot
double reciprocal plot
44
the vmax is more easily found on the lineweaver burk plot or the michaelis menten curve?
lineweaver burk plot
45
what is the vmax in the lineweaver burk plot
the intercept of the y axis is 1/vmax
46
on a lineweaver burk plot if your vmax has gone higher up on the y axis has your vmax increased or decreased?
decreased ==> bc reciprocal plot
47
the intercept on the x axis of the lineweaver burk plot is
-1/Km
48
lineweaver burk plot: as your x intercept approaches the origin, does your Km increase or decrease?
increase
49
covalent modification = irreversible inhibition
| give examples of GI enzymes
proinsulin ==> insulin
adding phosphates, sugars, OH groups
pepsinogen ==> pepsin
trypsinogen===> trypsin
50
ibuprofen (Advil) binds reversibly or irreversibly to COX
reversibly = therefore not covalent modification
51
aspirin binds reversibly or irreversibly to COX
irreversibly = aspirin adds acetyl group to the COX enzyme = covalent modification
52
any non protein molecule that assists an enzyme is called a
cofactor
53
cofactors can be metal ions or organic molecules. if a cofactor is organic it is specifically called a
coenzyme
54
Which is true:
all cofactors are coenzymes or
all coenzymes are cofactors?
all coenzymes are cofactors
not all cofactors are coenzymes
55
Km is a constant/or will it change
same = constant no matter how much enzyme you have
56
Vmax is a constant?
no it is not a constant it can change depending on how much enzyme you have. if you have more enzyme your vmax will be higher
57
changing enzyme concentration will affect Vmax or Km?
Vmax only
58
proteins that go all the way through the plasma membrane are called
integral proteins
59
proteins that are attached to one side or the other of the plasma membrane are called
peripheral proteins
60
integral proteins/peripheral proteins needs a detergent to isolate?
integral only. the peripheral do not need a detergent bc they fall off the membrane
61
name the 3 types of lipids in the plasma membrane
glycerophospholipids, sphingolipids and cholesterol
62
(phospholipids)
| aka glycerophospholipids are made up of
they have a glycerol backbone and 2 fatty acids,and a phosphate and an R group
63
the R groups differ in the glycerophospholipids what are the 5 phospholipids found in our membranes
```
phosphatidyl inositol
phosphatidylserine
phosphatidylcholine
phosphatidylethanolamine
phosphatidic acid
```
64
sphingolipids are made by?
sphingosine (hydrocarbon with an amino group) + Fatty acid ==> ceraminde ===> ceramide + sugar = glycosphingolipid
65
sphingosine + FA ==>
ceramide
66
sphingosine + FA + phosphocholine ==>
sphingomyelin
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sphingosine + FA + glucose ==>
glucosylcerebroside
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sphingosine + FA + oligosaccharide ==>
ganglioside
69
sphingomyelin found in many
nerve cell membranes
70
an inability to break down gangliosides give us what disease
Tay Sachs disease
71
1. Tay–Sachs disease is a rare autosomal recessive genetic disorder. it causes a progressive deterioration of nerve cells and of mental and physical abilities that begins around ___of age and usually results in death by the age of __.
2. The disease occurs when harmful quantities of cell membrane components known as gangliosides accumulate in the brain's nerve cells, eventually leading to the premature death of the cells.
six months
death = four years old
A ganglioside is a form of sphingolipid, which makes Tay–Sachs disease a member of the sphingolipidoses. There is no known cure or treatment.
72
cholesterol is important in maintaining the appropriate _ of the membrane
fluidity.
| Fluidity, strength, thickness, permeability and curvature of membrane
73
cholesterol has how many carbons and how many rings
27 carbons, 4 rings
74
cholesterol's role is __ dependent
temperature and concentration dependent
75
the more UNSATURATED/SATURATED fatty acids you have in a membrane the more fluid?
unsaturated fatty acids = more fluidity
76
simple diffusion needs
only a concentration gradient, small non polar O2 CO2 -----water is not non polar!! so it does not do simple diffusion
77
facilitated diffusion needs
membrane helper and concentration gradient
78
glucose gets into cell by
glucose transported = facilitated diffusion
79
primary active transport
moving against gradient, need ATP to fuel it and you need a protein helper
80
secondary active transport
moving against gradient, but do need ATP to fuel it and you need a protein helper. you use an established gradient
81
Epinephrine glucagon and ACTH are all stimulatory/inhibitory hormones for signal transduction pathways.
stimulatory = bind receptor = activates the G protein (Gs) = binds adenylyl cyclase ==> makes cAMP ==> makes protein kinase A
82
PGE1 and Adenosine are stimulatory/inhibitory hormones for signal transduction pathways.
inhibitory: bind receptor = activates the inhibiotry G protein (Gi) = which binds adenylyl cyclase ==> does not make cAMP ==>does not make protein kinase A
83
adenosine in our brain is responsible for
lack of motivation, tired. its receptors are blocked by caffeine
84
when cyclic AMP binds protein kinase A where does it bind and what happens
cyclic AMP binds the 2 regulatory units of PKA, which makes it release the catalytic units = ACTIVE PKA
85
what does protein kinase A do?
it adds phosphates = remember all kinases add phosphates
86
what enzyme degrades cAMP
phosphodiesterase
87
what can block the receptor in signal transduction?
arrestin
88
insulin uses a __ receptor
a catalytic tyrosine kinase receptor (RTK = receptor tyrosine kinase). it is a dimer, it binds insulin and acts like an enzyme on the cytoplasmic side. DOES NOT USE G PROTEIN
89
thyroid hormones and steroid hormones bind their receptors
inside the cell.
90
Growth hormone activates a cascade that activates
protein kinase C
| includes calcium
91
Ach uses?
neurotransmitter linked to ion channel. AcH binds receptor --> activates G protein which hits a potassium channel and opens it (directly activates the channel)
92
nitric oxide (gases) pathway uses
cGMP and protein kinase G
93
cGMP are broken down by
phosphodiesterases
94
Viagra inhibits
phosphodiesterase that breaks down cGMP so that there is more vasodilation
95
you have to have free glucose (monosaccharide) to pass into blood from intestinal cells: where is the low/high concentration- in the intestines or in the enterocyte cell?
enterocyte cell has higher glucose than inside the small intestine. Na+ is higher in the intestine than in the enterocyte, so sodium comes in down its gradient and glucose piggybacks in = Na+ glucose cotransporter
96
the Na+ glucose cotransporter is called __ and is __ transport
SGLT1 = Sodium Glucose Transporter 1, secondary transport, brings glucose that we ate into the intestinal cell.
97
glucose inside the enterocyte crosses into the blood using which transporter and is _ transport
GLUT2 transport protein = facilitated transport bc going down its concentration gradient
98
Na/K pump keeps
high potassium inside the cells and high sodium outside the cell. 3Na+ out, 2K+ in.
99
pancreas has _ receptors for glucose
GLUT 2 transporter
