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19 Cards in this Set

  • Front
  • Back
the hexose monophosphate pathway
about how much glucose in the liver can be oxidized this way
up to 30%

usually used in anabolic tissue

primary function is to generate NADPH, remember nadph is anabolic nadh is catabolic
Two sections of the pentose phosphate pathway
oxidative part
G6p--> 6-phosphoglucono(delta)lactone (made NADPH)--> 6-phosphogluconate -->ribulose-5-phospate(made NADPH and CO2) <-->

G6P deH makes NADPH by making a lactone from G6P, this is made irreversible by splitting that lactone ring in the next reaction using 6-phosphoglucolactonase,

6-phosphogluconate deH makes NADPH by making ribulose 5-phosphate from the split lactone 6-phosphogluconate
nonoxidative part
step 1 and 2
ribulose 5-phosphate is either isomerized by phosphopentose isomerase to r5Phosphate or epimerized by phosphopentose epimerase to xylulose 5-phosphate

transketolase transfers a two C unit from X5phosphate to r5phosphate making glyceraldehyde-3-phosphate (GAP) and sedoheptulose 7-phosphate
nonoxidative step 3
so now you have your 7C and your 3C, transaldolase takes a three C chunk off of the 7C and transfers it to the 3C making

fructose-6-phosphate (glycolysis, positive homotropic allosteric regulator of PFK1)
and erythrose 4-phosphate
Net reaction of the non oxidative part of the pentose pathway
3 r5Phosphate --> 2 F6P and 1 glyceraldehyde 3Phosphate

how do you measure thiamin deficiency?
abnormally low transketolase activity in erythrocytes

TPP effect
large stimulation of transketolase in vitro following addition of thiamin
which enzyme in the pentose pathway nonoxidative requires a coenzyme and what is it?
transketolase requires TPP
G6PD deficiency
pathology and symptoms
most common enz def disease

methemoglobinemia and hemolytic anemia

G6P deH deficiency causes reduced NADPH and so glutathione is not in it's reduced form (GSH)
Glutathione (GSH peroxidase) - reduces disulfide bonds and H2O2, principle antioxidant defense, without it RBC's breakdown prematurely
G6PD deficiency
things that will aggravate it
X-linked (symptoms typically limited to males)

half lives of variants are reduced

Fava bean compounds are converted to strong oxidants
anti-malarials lead to higher oxidative stress

NOTE: heterozygotes females recieve a little malarial protection since plasmodium invades RBCs (beta-thallassemia does so too)
Metabolism of other sugars


galac +ATP --> Gluc1P + ADP
galactose + ATP --> alpha-D Galactose1P + ADP

galac1P uridylyltransferase: Galac1P + UDP gluc --> UDP galactose + G1P

UDP-glucose epimerase:
UDP galactose-->UDP-glucose

G1P is shunted into the glycogen synthesis pathway
metabolism of D-Fructose not in liver
hexokinase makes it F-6-P

hexokinase makes if MAnnose-6-P,
phosphomannose isomerase makes M6P --> F6P

NOTE: F6P can go into glycolysis or can be changed to G6P via phosphoglucose isomerase
D-fructose metabolism in liver
fructokinase makes it F1P (cant do F1P to G1P[glycogen])

aldolase B splits F1P (like it would F16P) making DHAP and glyceraldehyde

Glyceraldehyde can go straight into GAP via triose kinase or into glycerol
F1P conversion into glycerol
F1P aldolase split into DHAP and glyceraldehyde

glyceraldehyde made into glycerol via alcohol dehydrogenase(makes NAD)

glycerol --> glycerol 3P via glycerol kinase (uses ATP)

glycerol-3P --> DHAP via glycerol phosphate deH (makes NADH)
deficiency of fructokinase, benign, fructose in urine
hereditary fructose intolerance

no aldolase B (hepatic form of aldolase)

F1P accumulates in liver, depletes ATP (gluconeogenesis) and Pi levels (glycogenolysis), which causes HYPOGLYCEMIA

AMP deaminase is activated by decreased Pi resulting in more purine catabolism and uric acid formation (gout)
refresher on purine catabolism!
AMP and GMP to xanthine to uric acid
refresher on purine and pyrimidine anabolism!
ribose-5-Phosphate --> PRPP --> purine synthesis(glu, gly, asp, Tetra methyl form and pyrimidine synthesis (carbamoyl phosphate)
Most common cause of galactosemia
Uridylyltransferase deficiency
cataracts, jaundice liver damage,

alleviating problems of galactosemia, in ADULTS - alternate pathway of UDP-galactose formation

treatment - avoid lactose