Energy and Glycolysis Flashcards
what is gibb’s free energy
energy capable of doing work
what is enthalpy
the heat content of the reacting system
what is entropy
quantitative expression of the randomness or disorder in the system
deltaG=
deltaH - TdeltaS
if delta G is negative
net loss of free energy
spontaneous
exergonic
it is exergonic if
delta G is negative
if delta G is positive
Net Gain of Free Energy
Not Spontaneous
Endergonic
if it is endergonic
delta G is positive
draw graph of negative delta G
pg 6
draw graph of positive delta G
pg 6
what does H stand for
enthalpy
what does S stand for
entropy
the more positive S, the more
thermodynamically favorable rxn will be
how does positive S make rxn more favorable
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).
what does delta G tell us about the reaction
if it will take place, but can only tell based on initial and final states
standard delta G is energy change when reactants and products are at concenctrations of
1 mol/L
biochemical standard for delta G is energy change at what pH
7
look up delta G in my biochem book
lda;lfkj
do practice problems from my biochem gbook for delta G
fa;slkdf
delta G 0 =
-RT ln Keq
delta G = delta G0 +
RT ln [B]/[A]
negative delta G
favor product
log 1 =
0
what is so important about ATP
high energy phosphate bonds
draw ATP
pg 9
in the process of breaking phosphate bonds in ATP
energy is released
ATP reaction is highly
exergonic
when glucose is in tissues, tissues like the liver will do what with glucose
produce a polymer of glucose: glycogen
where does energy come from to turn glucose to glycogen
ATP
glucose to glucose 6 P is what kind of rxn
endergonic - need ATP
UTP is similar to
ATP - it has two high energy bonds
draw full chain for glucose to glycogen
pg 11
UDP glucose to glycogen is what kind of rxn
endergonic
UTP is used to
combine sugars
CTP is used for
lipid synthesis
GTP is used for
protein synthesis
ATP can be used to repair
UTP, CDP, GTP
it sacrifices itself to repair the other guys
cleavage of high energy bonds release energy b/c products are more
stable
2 ADP =
ATP + AMP
draw out glycolysis
pg 14
breaking of carbon bonds in foods yields
energy
glucose linked to another glucose via what bond
glycosidic bonds
when break glycosidic bonds what is delta G
negative - it is a spontaneous rxn
carbs contain how much energy
4 kcal/g
protein contains how much energy
4 kcal/g
fat contains how much energy
9 kcal/g
EtOH contains how much energy
7 kcal/g
how do we store energy
adipose triacylglycerol → fat
glycogen
protein
how much of body weight is fat
20%
how much of our calories is stored in fat
85%
the polymers in fat are highly
reduced
when you oxidize fat
you get energy
glycogen polymer used to release
glucose
what are the two kinds of glyogen energy used
liver glycogen
muscle glycogen
ribose 5-phosphate is needed to produce
nucleic acids
glucose used to do what
lots of things
extracellular matrix and cell wall
glycogen, starrch, sucrose s(storage)
(look on pg 19)
draw out alpha d glucopyranose
pg 19
draw out D-glucose
pg 19
draw out and Beta D glucospyranose
pg 19
glucose metabolism depends on what two hormones
insulin and glucagon
insulin and glucagon are produced by
pancreas
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”
glucagon does what
reverses with insulin does. mobilizes fuels, maintains blood glucose levels during fasting.
what cells in pancreas produce glucagon
alpha cells
as glucose levels rise what happens to insulin
rises
as glucose levels rise hat happens to glucagon
fall
alpha cells do what
secrete glucagon
beta cells do what
secrete insulin
alpha and beta cells are from
pancreas
draw out pathway of glucose regulation of insulin **
pg 25
what phosphorylates glucose to glucose 6 phosphate
glucokinase
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
draw out pathway of glucose regulation of insulin know this well!!!
pg 25
polymers of carbohydrates
amylose & amylopectin
look at and understand difference b/w different sugar rings
pg 28
is sucrose reducing sugar
no
reducing sugar contains
3 anomeric carbon
fiber traps
water
by trapping water, fiber
softens stool
fiber can also inhibit
absorption of cholesterol
fructose, galactose, glucose are all
monomers from sugars
monomer sugars get in through what protein
SGLT1
glucose is taken against
concentration gradient (secondary transport)
Fructose absorbed by
GLUT5
GLUT5 is in
endothelial cells
all 3 monomer sugars can be transfered by
GLUT2
if there are mutations in gene for SGLT1 what will happen
severe diahhrea and dehydration
GLUT4
insulin-sensitive transporter.
in presence of insulin, number of what transporter increases
GLUT4
is glucose transport into RB rate limiting
no
what happens when GLUT2 doesn’t work
Fanconi-Bickel syndrome
GLUT2 where is it located
liver
if GLUT2 doesn’t work what happens with liver
glucose is accumulated in it
liver is too large
what happens to kidney if GLUT2 doesn’t work correctly
kidney doesn’t function correctly
too much glucose in kidney
what does pancreas do regarding glucose
enses glucose level
baby pts with GLUT2 deficiency, what happens with pancreas
impairment
if glucose cannot get in pancreas, insulin not released, have hyperglyemia → diabetes
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
RBC depend on what for energy
glucose
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.
what is the only GLUT stimulated by insulin
GLUT4
if GLUT4 isn’t working right what develops
hyperglycemia
glucose passes into CSF via
GLUT1
neural cells take up glucose via
GLUT3
Sugar + O2 what is waste product
CO2 + H2O
why is sugar and O2 eneergy released in steps
to conserve the energy, and the intermediates can also be used for other things
glycolysis is taking glucose to
pyruvate
first five steps known as
priming the pump
what is priming the pump
making glucose more reactive
glycolysis takes place where
in all cells in the cytoplasm
glucose is catabolized to yield
pyruvate
pyruvate is oxidized in
TCA
when pyruvate is oxidized in TCA it produces
CO2 and NADH
in absence of O2, pyruvate is
reduced to lactate
how many regulatory steps in glycolysis
3
draw out glycolysis
pg 39
what is first step of glycolysis
phosphorylation of glucose
what is first regulatory step of glycolysis
1st one! glucose → phosphorylated
is step one reversible? in glycolysis
no, it is irreversible
rxns far from equilibrium are common points of
regulation
what two enzymes help us out with phosphorylating glucose
hexokinase (muscular tissues)
glucokinase
what is concentration of glucose
5 mm
is hexokinase or glucokinase usually used
hexokinase
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
glucokinae affinity for substrate
low
but has high capacity
what is Km for glucokinase
high (low affinity)
what is Vmax for glucokinase
high
glucokinase is inhibited by
fructose 6-P
hexokinase is inhibited by
G6p
the liver only uses glucokinase when
glucose levels are high
if glucose is interalized and processed to produce G6P and you accumulate F6P it does what
inhibits glucokinase - signals liver to stop glycolysis
mutation of glucokinase leads to
MODY and gestational diabetes
what is step two of glycolysis
G6P isomerised into fructose 6 P by PGI
what is PGI stand for
phosphoglucose isomerase
what is step 3 of glycolysis
F6P to Fructose 1,6-biphosphate by FPK-1
want it to have more energy
Is ATP needed for step 3
yes
what is the main regulatory point of glycolsysi
step 3
is step 3 reversible
no it is irreverislbe, it is a rate limiting step
ATP at low concentration in glycolysis (specifically step 3) is a
substrate
ATP at high concentration in glycolysis (specifically step 3) is a
inhibitor
why do cells use ATP as energy
in normal concentration it is 5 mm
it only has 10% change
why is AMP used as sensor
when anything changes it changes by 600%, it is very sensitive
PFK1 if mutations will have
rare form of glycogen storage disease: GSD-VII
what will accumulate if there is mutation in PFK1
fructose 6 P
glucose 6 P
glycogen
glucose 6 P is inhibitor of
glycogen
so ultimately if there is mutation in PFK1, what will ultimately happen
interfere with glycogen degradation, sp pt has accumulation of glycogen, splenomegaly
PFK1 is tightly
regulated
what increaes Fructose 2,6 bisP
insulin
go through glucose regulation in liver
pg 52
what is step 4 & 5 of glycolysis
cleavage of fructose 1,6-bisphosphate and isomerization
what does aldolase do
cleave fructose 1,6bisP into DHAP and glyceraldehyde 3-P
DHAP is isomerised into
glyceraldehyde 3-P
aldolase there are many
isozymes
each of two or more enzymes with identical function but different structure
aldolase A expressed where
embryo,skeletal muscle, RBC
GSD stand for
glycogen storage disease
Aldolae B is expressed where
liver
mutation in Aldolase B have
fructose intolerance
mutation in Aldolase A have
GSD
where is Aldolase C found
brain
what is step 6 in glycolysis
Glyceraldehyde 3-phosphate dehydrogenase (GAPDH)
step 6 is what kind of reaction
oxidation reduction
write out Glyceraldehyde 3-phosphate dehydrogenase mechanism
pg 56
arsenic toxicity is primariliy due to
inhibition of pyruvate dehydrogenase – see TCA Cycle.
what are steps 7-9 in glycolysis
phophoglycerate kinase, phosphoglycero mutase and enolase
pyruvate kinase is allosterically inhibited by
by ATP, acetyl-CoA, and long-chain fatty acids (all signs of an abundant energy supply),
what triggers activation of pyruvate kinase
and the accumulation of fructose 1,6-bisphosphate triggers its activation.
pyruvate kinase deficiency causes
hemolytic anemia
any defect of glycolytic pathway leads to
hemolytic anemia
when pyruvate kinase if not functioning well what is a cell that will esp. have issues
RBC - all ATP comes from glycolysis
pyruvate kinase deficiency increases levels of
2,3 bisphosphoglycerate
1,3bisphosphoglycerate is precurser fo
2,3bisphosphoglycerate
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.
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
lactic acid normally produced by
RBC
name three points of regulation for glycolysis
hexokinase
PFK1
PK
hexokinase has feedback control by
glucose 6-P
PFK1 activated by
AMP & fructose 2,6 bisP
PFK1 inhibited by
ATP & citrate
PK is activated by
fructose 1,6-bisP
PK is inhibited by
ATP
net aerobic glycolysis
2 pyruvate
2 ATP
2NADH
does the brain ever use anaerobic glycolysis
no
anaerobic metablism produces low amoutn of
ATP but its fast help
aerobic metb
help
what are three possible fates of pyruvate
lactate
Acetyl CoA
ethanol
high level NADH low levels NAD cells produce
lactate
lactic acid pKa
3.85
lactic acid is completely
dissociated - physiological pH of 7.4
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)
aerobic metbolism fast or slow?
slow
anaerobic metabolism fast or slow?
fast
bottom line: : if you have any problems with organelles that use O2 (mitochondria) you induce the formation
lactic acid
what kind of glycolysis in tumor cells
anaerobic
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
tryglycerol becomes
glycerol & palmitate
pg 16
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
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
starch is digested by
amylase
when starch is digested what does it yield
oligosaccharides, maltose & isomaltose
describe structure of amylose
linear glucose chains connected by α1→4 linkages*
describe the structure of amylopectin
branched glucose chains. linear glucose chains connected by α1→4 linkages, branch points are α1→6 linkages*
sucrose is mono or disaccharide
disaccharide*
sucrose is made up of
fructose & glucose*
what kind of bond connects fructose & glucose in sucrose
disaccharide*
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
*
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.*
are mono or disaccharides taken up by cells
only mono*
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)*
describe structure of Isomaltose*
glucose-glucose disaccharide connected by α1→6 linkages (ie. fragments of starch from the branch points of amylopectin only)
where is GLUT1 expressed
cell types with barrier functions
think BBB, and all the other barriers
where is GLUT2 expressed
high-capacity, low-affinity transporter
think liver, pancreas, intestine
what is the most important regulated step of glycolysis?
step 3, Fructose-6-phoshate to fructose 1,6-bisphosphate by FPK-1
PFK1 is allosterically inhibited by
ATP
PFK1 is allosterically activated by
AMP
draw mechanism of high glucagon and low insulin and how it affects PFK-2 and FBP-2
pg 52
draw mechanism of high insulin and low glucagon and how it affects PFK-2 and FBP-2
pg 52
arsenic poisioning starts where
cytosol
Arsenic toxicity is primarily due to the inhibition
pyruvate dehydrogenase
high NADH/NAD+ ration favors production of what
lactate
in the heart and liver the low NADH/NAD+ ratio favor production of what
oxidation of lactate to pyruvate
anaerobic glycolysis (like if O2 isn’t getting to tissues) produces
lactate→lactic acidosis
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.
