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61 Cards in this Set

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glycolysis
pathway by which glucose is converted to pyruvate
occurs in
cytosol
produces
ATP, NADH, pyruvate
any disruption to glycolysis process will first be seen in
erythrocytes e.g. hemolytic anemia
hemolytic anemia
F- poisoning. spleen will be overworked trying to break down "broken" erythrocytes, and liver will be overworked trying to produce new ones
how does glucose travel across cell membrane?
on a transport protein (insulin stimulates glucose transport into muscle and adipose tissue cells).
erythrocytes are missing mitochondria in what areas of the pathway?
TCA cycle and e- transport chain, so glycolysis is only energy producing pathways for them.
step 1.
1. glucose to glucose-6-phosphate

g--> g-6-p
enzyme to step 1
hexokinase IV (aka Glucokinase) in liver (*kinases phosphorylate things)
step 1: does ATP hydrolyze to ADP? ..if so, what cofactor is needed everytime ATP is a substrate?
yes...Mg++ is cofactor-tweaks ATP just right so that enzyme can identify it
if ATP-->ADP and Mg++ is used...what harmful effect can take place?
F- poisoning (F- ties up the Mg++)
regulation of step 1:

1.
2.
1.hexokinases stimulated by glucose and insulin, but not glucokinase-otw liver would suck up alll the glucose.
2. hexokinases are inhibited by glucagon and G-6-P (not in the case of glucokinase)
glycolysis step 1.
rate limiting step and irreversible
Km

lower Km
higher Km
[s] substrate conc. where velocity is half maximal

lower Km = higher affinity
higher Km = lower affinity... the more substrate u need to have to get Vmax/2
glucokinase has a higher or lower Km? b/c...
glucokinase has a higher Km, so that the cells can take up glucose before the liver
step 2:
Glucose-6-phosphate to Fructose-6-phosphate (isomers)
step 2: enzyme
phosphoglucoisomerase aka phosphofructoisomerase
step 3:
fructose-6-phosphate to
fructose-6-phosphate to fructose 1,6 bisphosphate
step 3: enzyme
1.does ATP --> ADP?
2. anything else?
phosphofructokinase I (PFK I)

-yes..(phosphate added to substrate)..so Mg++ is needed and potential F- poisoning

-MAJOR RATE LIMITING/IRREVERSIBLE STEP
-FIRST COMIMITTED STEP IN THE PATHWAY)
1.insulin:glucagon is important here
insulin: glucagon

ratio high?
ratio low?
ratio high = increase PFK 1 to continue rxn

insulin increase: glucagon (store energy)-->stim. fatty acid synthesis

ratio low = no PFK 1 cell production
regulation of step 3:

1.
2.
1.in muscle: PFK 1 is activated by AMP and inhibited by ATP and citrate
2. in liver, PFK 1 is activated by fructose 2,6-bisphosphate
step 4: fructose 1,6 bisphosphate to
fructose 1,6 bisphosphate is cleaved into 2 molecules
step 4: fructose 1, 6 bisphosphate is...
cleaved into 2 molecules: DHAP and PGAL
step 4 f-1,6,bis-p to DHAP and PGAL ...enzyme:
aldolase A...not necessarily 1:1 ratio!!!
step 4: if lots of energy, rxn favors? if low energy...
DHAP (low insulin:glucagon), which can be used as backbone for triglycerides. DHAP is used for storage. muscles are consumers so not much DHAP to be found...
..if low energy..PGAL is favored (high insulin:glucagon)

*for the 38ATP produced from one molecule of glucose, assume u get 2 molecules of PGAL...
what is the enzyme that isomerizes between PGAL and DHAP?
trios-phosphate-isomerase
step 5: 2 PGAL to ?

enzyme-glyceraldehyde phosphate dehydrogenase (PGAL dehydrogenase)
2 1,3 bisphosphoglycerate
step 5: pgal to 1,3 bisphosphoglycerate enzyme?
glyceraldehyde phosphate dehydrogenase (PGAL dehydrogenase)
dehydrogenase indicates:
to add or remove a proton, so NAD (niacin) is involved

-NAD is reduced to NADH (gain of 2 NADH) ...body produces Niacin, but only 2%, so we need to consume Niacin
arsenic poisoning?

stops glycolysis where?

-prods or causes: 1 and 2
can take place of phosphate group, they look similar. although PGAL dehydrogenase is forgiving and allows rxn to proceed.

phosphoglycerate kinase is very tight and will pathway if arsenic takes place of phosphate group

-1-arsenato,3-phosphoglcerate, at C1

-causes hemolytic anemia and hepato-, slenomegaly and liver enlargement
step 6: 2 1, 3 bisphosphoglycerate to ? with enzyme phosphoglycerate kinase
2 3-phosphoglycerate

*gain of 2 ADP --> 2 ATP
*RBC Shunt (no ATP PRODUCED)
step 6: 2 1, 3 bisphosphoglycerate to 2 3-phosphoglycerate with ? enzyme
phosphoglycerate kinase-cannot recognize molecule if arsenic is attached
part of step 6: 1,3 bisphosphoglycerate--> 2, 3 bisphosphoglycerate with enzyme b-p-g mutase --> 3 p-g with bis-p-g mutase...why's this step necessary?
this step is necessary for erythrocytes b/c 2,3 bis-p-g keeps O2 from being reabsorbed by the erythrocytes as they pass thru the capillaries (otw u'll suffocate)
-erythrocytes will break down if o.b.c is not down
-myoglobin binds O2 at lower partial pressure
what are 3 steps in glycolysis that cause hemolytic anemia?
hexokinase (step 1), PFK1, enolase(directly)
what three things lower O2 in RBC shunt(good thing!)
1. 2,3 bisphosphoglycerate
2. protons
33. CO2
step 7: 2 3-phosphoglycerate to 2 2-phosphoglycerate with ? enzyme
phosphoglyceromutase
step 8: 2 2-p-g to 2 p-enol-pyruvate (PEP) with ? enyzme
enolase-directly inhibited by halogends, so this is another place where F- can interfere
-water molecules leave
step 9: final step!!!

2 PEP to Pyruvate with ? enzyme
pyruvate kinase

2 ADP --> 2 ATP
pyruvate kinase is stimulated by? (2 things) and inhibited by? (2 things)
stimulated by insulin and fructose 1, 6 bisphosphate

-inhibited by alanine and glucagon
how many net ATP produced in complete breakdown of glycolysis?

in anaerobic conds? why?
net 8 ATP per/1 mole of glucose

net 2 ATP b/c don't want pyruvate to go into mitochondria
-divert C's of pyruvate away from mitochondria to lactate --> 2 mole of lactate

2 NADH--> 2 NAD+ instead of--> ATP so -2 NADH or -6 ATP
hypoxia?
O2 deficit, run and can't get enuf O2. produce lots of H+ (protons) and attaches to make H2O
-pH ddrops and u acidify to death
summary: which steps produce ADP?

which steps produce ATP?
hexokinase and phosphofructokinase-1 (PFK1)

phosphoglycerate kinase and pyruvate kinase
which step is the first committed step?
PFK1 to fructose 1, 6 bisphosphate
which step will not occur if arsenic poisoning?
phosphoglycerate kinase

rbc shunt occurs here as well
PFK 1 will function at a high or low rate when blood glucose is high or low?
at a high rate when blood glucose is high, or in cells when there is a need for ATP
anytime u have a prob wit glycolysis, u have what type of deficiency?
pyruvate kinase deficiency- blocks glycolytic pathway
PFK 1 is activated by ?
is activated by fructose 2, 6 bisphosphate which, is formed from fructose 6 phosphate by PFK 2 when insulin is high, PFK 1 is stimulated by product of PFK2
in fasting state, when glucagon is elevated, PFK2 is phosphorylated by protein kinase A which is activated by cAMP. when this happens what happens to PFK1?
when PFK2 is phosphorylated it converts 2,6 bisphosphate back to fructose-6-phosphate therefore making PFK1 less active
when insulin is high, PFK2 is dephosphorylated making it more active in producing 2, 6-bisphosphate which does what for PFK 1?
when insulin is high, and PFK2 is dephosphorylated, making it more active in producing 2, 6-b-p, it stimulates PFK 1.
PFK2 is under the control of ? in blood

PFK 1 is under stimulation of only things going on where?
of I:G ratio in blood and PFK 1 is under stimulation of things within the cell.
PFK 2 is a dimer..what is a dimer?
-in fed state, PFK2 acts as a ?
-in fasting state?
PFK2 acts as two enzymes stuck together...acts as a kinase in the fed state when it is dephosphorylated and as a phosphotase in the fasting state when it is phosphorylated.
PFK 1 and PFK 2 have ___ substrates, which are ____ and _____, but ___ products.
have common substrates (ATP and fructose - 6- phosphate) but different products
How does I:G ratio regulate phosphorylation of enzymes?
-what triggers the mechanism?
-what enzyme is stimulated by this? ..and what does it do?
-glucagon directly triggers mechanism by attaching to its receptor sites
-adenylate cyclase, which converts ATP to cAMP, which stimulates protein kinases (whose job is to phosphorylate things) to PFK 2
what does glucagon do?

if something is stimulated by glucagon, then ___ active when phosphorylated, if something is inhibited by glucagon, the you know it is ___ active when phosphorylated.
it phosphorylates things. if it is stimulated by glucagon then u know it is more active when phosphorylated. if it is inhibited by glucagon (glycolysis rxns), then you know it is less active when phosphorylated.
I:G up, __ glucose in blood stream

up insulin; __ phosphorylation

down insulin; __ phosphorylation
up glucose in blood stream

down phosphorylation

up glucagon-phosphorylation
phosphotase is ?
removing phosphates to make PFK II active
Michealis-Menten Eaquation
describes affinity of an enzyme to a substrate
-can be used to compare diff enzymes' affinity to the same substrate
km=(s) where velocitty is half maximal
-if he gives u 2 diff substrates, u would not be able to apply this...CAN ONLY COMPARE ONE SUBSTRATE!
example of Michealis-Menten
hexokinase vs glucokinase: as glucose travels thru bloodstream, its first stop is the liver. u don't want the liver to suck up all the glucose and utilize it for itself so it has an enzyme that has a lower affinity to the substrate glucose. it follows that glucokinase has a higher Km than does hexokinase! Hexokinase and Glucokinase are isoenzymes.
anaerobic glycolysis is what two steps?..pyruvate to ? and then pyruvate to ?

-what enzyme?
-what happens to NADH?
pyruvate to lactate (still in cytosol

-lactate dehydrogenase
-NADH-->NAD+ (vitamin: Niacin)
-NADH, which is produced by glycolysis, must be reconverted to NAD+, so that the carbons of glucose can continue to flow thru glycolysis...

-pyruvate to alanine

-alanine and lactate go out into blood travel to liver, and if energy is needed will be converted back to glucose via gluconeogenesis
pyruvate to alanine
coupled with?
enzyme used/vit. used?
example of what kind of rxn?
-what is alpha keto form of...
1. alanine?
2.glutamate?
3.aspartate?
coupled with glutamate to alpha-keto gluterate
-enzyme: transaminase (vit. pyridoxine)
-this is an example of a transamination rxn
1.pyruvate
2.alpha keto gluterae
3.OAA (oxaloacetate)
glucagon vs. epinephrine


glucagon has _____ on muscle tissue

-glycogen in liver provides glucose for blood so muscle tissue can continue
-no effect

epinephrine provides glucagon without going into the blood stream...delayed response vs glycogen...