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17 Cards in this Set
- Front
- Back
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gluconeogenesis
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reverse of glycolysis EXCEPT there are three irreversible reactions that must be overcome through the use of different gluconeogenic enzymes
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glycolysis
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usually go from glucose to pyruvate, now want to start with pyruvate/aa/lactate and work backwards
glycolysis backwards pyruvate--> PEP--. 2-phosphoglycerate-->3phosphoglycerate-->1,3bPglycerate --> GAP --> F1,6bP --> F6P --> G6P --> G |
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Bypass step 1
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pyruvate + ATP + HCO3 --> oxaloacetate (is transported out of mito via malate shuttle) + GTP --> PEP + CO2 + Pi
Coupling of carboxy then decarboxy reactions Pyruvate carboxylase, then PEPCK (PEP carboxy kinase) NOTE: anapleurotic because makes OAA a TCA interm |
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Describe Pyruvate carboxylase
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In mito
biotin coenz cov linked to lys which allows it to swing between active sites in the enz biotin attaches a CO2 in one active site, swings and transfers carboxy group to pyruvate in another active site can also carboxlate acetyl and propionyl |
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Pyruvate Carboxylase regulation
activation inhibition pyruvate kinase control in comparison? |
Allosteric activation: Acetyl CoA (a product of FA metabolism, it also inhibits PDH by activating PDH kinase)
makes sense if gluc is low, FA will be metabolized and want gluconeogenesis, not PDH leading to TCa cycle NOTE: allosterically inhibited by aspartate, inhib by ADP Pyruvate kinase is pos F16P and neg ATP |
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Steps leading up to Bypass 2
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PEP --> 2 phosphoglycerate-->3phosphoglycerate--> 1,3bPglycerate-->GAP-->F1,6P
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Bypass step 2
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F1,6bP --> F6P
hydrolising the phosphate ester F1,6bphosphatase, uses H2O |
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regulation of F1,6bPhosphatase
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inhibited allosterically by F2,6P and AMP
F2,6P activates reverse reaction (therefore its a reciprocal regulator) activated by citrate NOTE: PFK1 is positively activated by AMP and F26P and neg inhib by ATP and citrate |
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Bypass 3
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G6P --> G
hydrolyzed by glucose 6Phosphatase membrane bound in ER, only found in liver and kidney, so no other tissue can release free glucose, high Km, will only function when G6P is high utilizes water |
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Glucose 6-Phosphatase and the ER
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G6P transported into ER where enz can hydrolyze it, Gluc and Pi are in lumen and need to be transported back out
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Glycogen storage disease Ia
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deficiency of glucose-6-phosphatase
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gluconeogenesis overall
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converts two pyruvate to one glucose, consuming 2 NADH amd 6 ATP/GTP
vs glycolysis which makes 2 nadh and 2 ATP |
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how do you get NADH in cytosol to fuel gluconeogenesis
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See page 57
pyruvate into mit pyruvate to OAA OAA to malate producing NAD malate out malate to OAA producing NADH important to have NADH in cytosol for use in gluconeogenesis normally NADH/NAD cytosolic ratio is usually very low |
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LACTATE and gluconeogenesis (from RBC and muscle)
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lactate is converted to pyruvate in the cytosol yeilding NADH (no need for transport to make cytosolic NADH)
pyruvate is then shuttled into cell goes through the normal pathway (--> OAA via pyruvate carboxylase) --> PEP via PEPCK happens in mito! as oppose to in cytosol of regular pyruvate metab PEP can leave cell or OAA can --> asp via transamination, asp can leave directly NEITHER ROUTE EXPORTS REDUCING EQUIV OAA in mito can leave directly via asp or can be converted to PEP by PEP carboxykinase which can be exported to cytosol |
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alanine makes?
glutamine makes? |
ala --> pyruvate
glutamine --> alphaketo glutarate |
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The Cori cycle
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glycolysis in muscle makes 2ATP and 2 Lactate
those lactates go to liver liver puts two lactates through gluconeogenesis using 6ATP to make glucose glucose is then released |
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how much ATP is required for gluconeogenesis in liver?
how much ATP is generated from gluc in muscle |
6ATP required to make glucose in liver and 2NADH
2ATP generated from glucose in anaerobic muscle/ 36ATP in aerobic |
