Energy and Glycolysis Flashcards
1
Q
what is gibb’s free energy
A
energy capable of doing work
2
Q
what is enthalpy
A
the heat content of the reacting system
3
Q
what is entropy
A
quantitative expression of the randomness or disorder in the system
4
Q
deltaG=
A
deltaH - TdeltaS
5
Q
if delta G is negative
A
net loss of free energy
spontaneous
exergonic
6
Q
it is exergonic if
A
delta G is negative
7
Q
if delta G is positive
A
Net Gain of Free Energy
Not Spontaneous
Endergonic
8
Q
if it is endergonic
A
delta G is positive
9
Q
draw graph of negative delta G
A
pg 6
10
Q
draw graph of positive delta G
A
pg 6
11
Q
what does H stand for
A
enthalpy
12
Q
what does S stand for
A
entropy
13
Q
the more positive S, the more
A
thermodynamically favorable rxn will be
14
Q
how does positive S make rxn more favorable
A
Ie a positive ΔS tends to make ΔG more negative or exergonic. This is why an ice cube will melt spontaneously at room temperature (the water molecules are becoming more disordered or gaining entropy) even though ice melting is an endothermic reaction (absorbs heat energy).
15
Q
what does delta G tell us about the reaction
A
if it will take place, but can only tell based on initial and final states
16
Q
standard delta G is energy change when reactants and products are at concenctrations of
A
1 mol/L
17
Q
biochemical standard for delta G is energy change at what pH
A
7
18
Q
look up delta G in my biochem book
A
lda;lfkj
19
Q
do practice problems from my biochem gbook for delta G
A
fa;slkdf
20
Q
delta G 0 =
A
-RT ln Keq
21
Q
delta G = delta G0 +
A
RT ln [B]/[A]
22
Q
negative delta G
A
favor product
23
Q
log 1 =
A
0
24
Q
what is so important about ATP
A
high energy phosphate bonds
25
draw ATP
pg 9
26
in the process of breaking phosphate bonds in ATP
energy is released
27
ATP reaction is highly
exergonic
28
when glucose is in tissues, tissues like the liver will do what with glucose
produce a polymer of glucose: glycogen
29
where does energy come from to turn glucose to glycogen
ATP
30
glucose to glucose 6 P is what kind of rxn
endergonic - need ATP
31
UTP is similar to
ATP - it has two high energy bonds
32
draw full chain for glucose to glycogen
pg 11
33
UDP glucose to glycogen is what kind of rxn
endergonic
34
UTP is used to
combine sugars
35
CTP is used for
lipid synthesis
36
GTP is used for
protein synthesis
37
ATP can be used to repair
UTP, CDP, GTP
| it sacrifices itself to repair the other guys
38
cleavage of high energy bonds release energy b/c products are more
stable
39
2 ADP =
ATP + AMP
40
draw out glycolysis
pg 14
41
breaking of carbon bonds in foods yields
energy
42
glucose linked to another glucose via what bond
glycosidic bonds
43
when break glycosidic bonds what is delta G
negative - it is a spontaneous rxn
44
carbs contain how much energy
4 kcal/g
45
protein contains how much energy
4 kcal/g
46
fat contains how much energy
9 kcal/g
47
EtOH contains how much energy
7 kcal/g
48
how do we store energy
adipose triacylglycerol → fat
glycogen
protein
49
how much of body weight is fat
20%
50
how much of our calories is stored in fat
85%
51
the polymers in fat are highly
reduced
52
when you oxidize fat
you get energy
53
glycogen polymer used to release
glucose
54
what are the two kinds of glyogen energy used
liver glycogen
| muscle glycogen
55
ribose 5-phosphate is needed to produce
nucleic acids
56
glucose used to do what
lots of things
extracellular matrix and cell wall
glycogen, starrch, sucrose s(storage)
(look on pg 19)
57
draw out alpha d glucopyranose
pg 19
58
draw out D-glucose
pg 19
59
draw out and Beta D glucospyranose
pg 19
60
glucose metabolism depends on what two hormones
insulin and glucagon
61
insulin and glucagon are produced by
pancreas
62
insulin is a hormone that when secreted body is teling tissue
"we have just eaten, we are going to put this away, produce glycogen, fat, and do protein synthesis"
63
glucagon does what
reverses with insulin does. mobilizes fuels, maintains blood glucose levels during fasting.
64
what cells in pancreas produce glucagon
alpha cells
65
as glucose levels rise what happens to insulin
rises
66
as glucose levels rise hat happens to glucagon
fall
67
alpha cells do what
secrete glucagon
68
beta cells do what
secrete insulin
69
alpha and beta cells are from
pancreas
70
draw out pathway of glucose regulation of insulin ****
pg 25
71
what phosphorylates glucose to glucose 6 phosphate
glucokinase
72
what does it mean that glucokinase has high Km
low affinity for glucose - it's good b/c you only want it to work when glucose levels are high
73
draw out pathway of glucose regulation of insulin know this well!!!
pg 25
74
polymers of carbohydrates
amylose & amylopectin
75
look at and understand difference b/w different sugar rings
pg 28
76
is sucrose reducing sugar
no
77
reducing sugar contains
3 anomeric carbon
78
fiber traps
water
79
by trapping water, fiber
softens stool
80
fiber can also inhibit
absorption of cholesterol
81
fructose, galactose, glucose are all
monomers from sugars
82
monomer sugars get in through what protein
SGLT1
83
glucose is taken against
concentration gradient (secondary transport)
84
Fructose absorbed by
GLUT5
85
GLUT5 is in
endothelial cells
86
all 3 monomer sugars can be transfered by
GLUT2
87
if there are mutations in gene for SGLT1 what will happen
severe diahhrea and dehydration
88
GLUT4
insulin-sensitive transporter.
89
in presence of insulin, number of what transporter increases
GLUT4
90
is glucose transport into RB rate limiting
no
91
what happens when GLUT2 doesn't work
Fanconi-Bickel syndrome
92
GLUT2 where is it located
liver
93
if GLUT2 doesn't work what happens with liver
glucose is accumulated in it
| liver is too large
94
what happens to kidney if GLUT2 doesn't work correctly
kidney doesn't function correctly
| too much glucose in kidney
95
what does pancreas do regarding glucose
enses glucose level
96
baby pts with GLUT2 deficiency, what happens with pancreas
impairment
| if glucose cannot get in pancreas, insulin not released, have hyperglyemia → diabetes
97
GLUT1 deficiency affects
| explain
brain
the brain needs a lot of glucose, if you impair glucose getting to BBB, you are affecting brain. all symptoms are brain impairment
98
RBC depend on what for energy
glucose
99
why does pt not die if they have GLUT1 deficiency
redundancy mechanisms, if something doesn't work there is plan B.
sometimes these mechanisms compensate to normality, sometimes they don't.
100
what is the only GLUT stimulated by insulin
GLUT4
101
if GLUT4 isn't working right what develops
hyperglycemia
102
glucose passes into CSF via
GLUT1
103
neural cells take up glucose via
GLUT3
104
Sugar + O2 what is waste product
CO2 + H2O
105
why is sugar and O2 eneergy released in steps
to conserve the energy, and the intermediates can also be used for other things
106
glycolysis is taking glucose to
pyruvate
107
first five steps known as
priming the pump
108
what is priming the pump
making glucose more reactive
109
glycolysis takes place where
in all cells in the cytoplasm
110
glucose is catabolized to yield
pyruvate
111
pyruvate is oxidized in
TCA
112
when pyruvate is oxidized in TCA it produces
CO2 and NADH
113
in absence of O2, pyruvate is
reduced to lactate
114
how many regulatory steps in glycolysis
3
115
draw out glycolysis
pg 39
116
what is first step of glycolysis
phosphorylation of glucose
117
what is first regulatory step of glycolysis
1st one! glucose → phosphorylated
118
is step one reversible? in glycolysis
no, it is irreversible
119
rxns far from equilibrium are common points of
regulation
120
what two enzymes help us out with phosphorylating glucose
hexokinase (muscular tissues)
| glucokinase
121
what is concentration of glucose
5 mm
122
is hexokinase or glucokinase usually used
hexokinase
123
when is glucokinase used
when we eat and glucose is increased - affinity for substrate is low but once it gets going the velocity takes off
124
glucokinae affinity for substrate
low
| but has high capacity
125
what is Km for glucokinase
high (low affinity)
126
what is Vmax for glucokinase
high
127
glucokinase is inhibited by
fructose 6-P
128
hexokinase is inhibited by
G6p
129
the liver only uses glucokinase when
glucose levels are high
130
if glucose is interalized and processed to produce G6P and you accumulate F6P it does what
inhibits glucokinase - signals liver to stop glycolysis
131
mutation of glucokinase leads to
MODY and gestational diabetes
132
what is step two of glycolysis
G6P isomerised into fructose 6 P by PGI
133
what is PGI stand for
phosphoglucose isomerase
134
what is step 3 of glycolysis
F6P to Fructose 1,6-biphosphate by FPK-1
| want it to have more energy
135
Is ATP needed for step 3
yes
136
what is the main regulatory point of glycolsysi
step 3
137
is step 3 reversible
no it is irreverislbe, it is a rate limiting step
138
ATP at low concentration in glycolysis (specifically step 3) is a
substrate
139
ATP at high concentration in glycolysis (specifically step 3) is a
inhibitor
140
why do cells use ATP as energy
in normal concentration it is 5 mm
| it only has 10% change
141
why is AMP used as sensor
when anything changes it changes by 600%, it is very sensitive
142
PFK1 if mutations will have
rare form of glycogen storage disease: GSD-VII
143
what will accumulate if there is mutation in PFK1
fructose 6 P
glucose 6 P
glycogen
144
glucose 6 P is inhibitor of
glycogen
145
so ultimately if there is mutation in PFK1, what will ultimately happen
interfere with glycogen degradation, sp pt has accumulation of glycogen, splenomegaly
146
PFK1 is tightly
regulated
147
what increaes Fructose 2,6 bisP
insulin
148
go through glucose regulation in liver
pg 52
149
what is step 4 & 5 of glycolysis
cleavage of fructose 1,6-bisphosphate and isomerization
150
what does aldolase do
cleave fructose 1,6bisP into DHAP and glyceraldehyde 3-P
151
DHAP is isomerised into
glyceraldehyde 3-P
152
aldolase there are many
isozymes
| each of two or more enzymes with identical function but different structure
153
aldolase A expressed where
embryo,skeletal muscle, RBC
154
GSD stand for
glycogen storage disease
155
Aldolae B is expressed where
liver
156
mutation in Aldolase B have
fructose intolerance
157
mutation in Aldolase A have
GSD
158
where is Aldolase C found
brain
159
what is step 6 in glycolysis
Glyceraldehyde 3-phosphate dehydrogenase (GAPDH)
160
step 6 is what kind of reaction
oxidation reduction
161
write out Glyceraldehyde 3-phosphate dehydrogenase mechanism
pg 56
162
arsenic toxicity is primariliy due to
inhibition of pyruvate dehydrogenase – see TCA Cycle.
163
what are steps 7-9 in glycolysis
phophoglycerate kinase, phosphoglycero mutase and enolase
164
pyruvate kinase is allosterically inhibited by
by ATP, acetyl-CoA, and long-chain fatty acids (all signs of an abundant energy supply),
165
what triggers activation of pyruvate kinase
and the accumulation of fructose 1,6-bisphosphate triggers its activation.
166
pyruvate kinase deficiency causes
hemolytic anemia
167
any defect of glycolytic pathway leads to
hemolytic anemia
168
when pyruvate kinase if not functioning well what is a cell that will esp. have issues
RBC - all ATP comes from glycolysis
169
pyruvate kinase deficiency increases levels of
2,3 bisphosphoglycerate
170
1,3bisphosphoglycerate is precurser fo
2,3bisphosphoglycerate
171
if there are high levels of 2,3bisphosphoglycerate what happens to delivery of oxygen
delivery of oxygen improves, so it is compensating. so the hemoglboin pt does have works better.
172
if there is a problem with the enzymes leading to 1,3bisphoshpoglycerate what happens to delivery of oxygen
2,3bisphophoglycerate decreases so delivery of oxygen decreases. so if they also have pyruvate kianse defiicency they don't have enough oxygen and they have anemia, and they also dont have compensatory mechanism
173
lactic acid normally produced by
RBC
174
name three points of regulation for glycolysis
hexokinase
PFK1
PK
175
hexokinase has feedback control by
glucose 6-P
176
PFK1 activated by
AMP & fructose 2,6 bisP
177
PFK1 inhibited by
ATP & citrate
178
PK is activated by
fructose 1,6-bisP
179
PK is inhibited by
ATP
180
net aerobic glycolysis
2 pyruvate
2 ATP
2NADH
181
does the brain ever use anaerobic glycolysis
no
182
anaerobic metablism produces low amoutn of
ATP but its fast help
183
aerobic metb
help
184
what are three possible fates of pyruvate
lactate
Acetyl CoA
ethanol
185
high level NADH low levels NAD cells produce
lactate
186
lactic acid pKa
3.85
187
lactic acid is completely
dissociated - physiological pH of 7.4
188
in absense of mitochondria or O2 what happens to NADH
it is oxidized to NAD+ by reduction of pyruvate to lactate catalysed by lactate dehydrogenase (LDH)
189
aerobic metbolism fast or slow?
slow
190
anaerobic metabolism fast or slow?
fast
191
bottom line: : if you have any problems with organelles that use O2 (mitochondria) you induce the formation
lactic acid
192
what kind of glycolysis in tumor cells
anaerobic
193
how does PET test work
basically light up the glucose in the body
| pt ingests the modified glucose, tmor cells take a lot of it, and then can view in pet scan
194
tryglycerol becomes
glycerol & palmitate
| pg 16
195
describe the glucoregulation process in α cells
increase in plasma glucose → cell generates ATP → ATP closes K+ channels → depolarization → Ca2+ and Na+ channels activated → blocks exocytosis (which would contain glucagon)
pg 27
196
describe the glucoregulation process in ß cells
increase in plasma glucose → cell generates ATP → ATP closes K+ channels → depolarization → Ca2+ channels activated → release insulin via exocytosis
197
starch is digested by
amylase
198
when starch is digested what does it yield
oligosaccharides, maltose & isomaltose
199
describe structure of amylose
linear glucose chains connected by α1→4 linkages*
200
describe the structure of amylopectin
branched glucose chains. linear glucose chains connected by α1→4 linkages, branch points are α1→6 linkages*
201
sucrose is mono or disaccharide
disaccharide*
202
sucrose is made up of
fructose & glucose*
203
what kind of bond connects fructose & glucose in sucrose
disaccharide*
204
is sacrose a reducing sugar? why or why not?
no
Sucrose is non reducing sugar because the anomeric carbon from fructose and glucose are used to form a glycosidic bond
*
205
is lactose a reducing sugar? why or why not?
yes
since only one anomeric carbon is used to form a glycosidic bond. The other anomeric carbon can open and close giving rise the reducing properties.*
206
are mono or disaccharides taken up by cells
only mono*
207
describe structure of maltose
Maltose – a glucose-glucose disaccharide connected by α1→4 linkages (ie. fragments of the linear chains of starch – either amylose or amylopectin)*
208
describe structure of Isomaltose*
glucose-glucose disaccharide connected by α1→6 linkages (ie. fragments of starch from the branch points of amylopectin only)
209
where is GLUT1 expressed
cell types with barrier functions
| think BBB, and all the other barriers
210
where is GLUT2 expressed
high-capacity, low-affinity transporter
| think liver, pancreas, intestine
211
what is the most important regulated step of glycolysis?
step 3, Fructose-6-phoshate to fructose 1,6-bisphosphate by FPK-1
212
PFK1 is allosterically inhibited by
ATP
213
PFK1 is allosterically activated by
AMP
214
draw mechanism of high glucagon and low insulin and how it affects PFK-2 and FBP-2
pg 52
215
draw mechanism of high insulin and low glucagon and how it affects PFK-2 and FBP-2
pg 52
216
arsenic poisioning starts where
cytosol
217
Arsenic toxicity is primarily due to the inhibition
pyruvate dehydrogenase
218
high NADH/NAD+ ration favors production of what
lactate
219
in the heart and liver the low NADH/NAD+ ratio favor production of what
oxidation of lactate to pyruvate
220
anaerobic glycolysis (like if O2 isn't getting to tissues) produces
lactate→lactic acidosis
221
under low oxygen conditions, describes what happens with HIF (esp. in regards to tumor)
if low oxygen, more HIF. HIF is TF.
| increases production of glucose transporters.
