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12 Cards in this Set

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What is the mechanism of the PDH reaction?
--Converts Pyruvate-->Acetyl CoA
--"Handing off" of one intermediate between subunits.
--3 complexes--pyruvate dehydrogenase (PDH), dihydrolipoyl transacetylase (DHT), and dihydrolipoyl dehydrogenase (DHD)

1) PDH removes CO2 from pyruvate and transfers remaining carbon chain to TPP, forming an intermediate.
2) PDH/DHT oxidize the intermediate to acetate moiety and transfer it to lipoamide-->makes acetate portion reactive with CoA.
3) DHT transfers acetate to CoA-->makes Acetyl CoA.
3) DHD oxidizes lipoamide (transfers electrons to FAD) and oxidizes FAD (transfers electrons to NAD)-->regenerates both lipoamide and FAD for another rxn.
What are some big points about the TCA cycle?
1) carbons lost (as CO2) means you can never have gluconeogenesis from Acetyl CoA.
2) A GTP is generated (by substrate level phosphorylation)
3) NADH is produced by 3 rxns, FADH2 by 1 rxn.
4) alpha-ketoglutarate dehydrogenase reaction is SAME mechanism as PDH.
5) malate dehydrogenase rxn favors malate production (instead of OAA)-->so, cell decreases OAA and NADH, so malate will make more OAA!
What are steps in TCA cycle? (you need to know this, the enzymes, and where NADH/FADH2 is made)
ACETYL COA+OAA--(citrate synthase)-->CITRATE--(aconitase)-->CIS-ACONITATE--(aconitase)-->ISOCITRATE--(isocitrate dehydrogenase--NADH MADE)-->OXALOSUCCINATE--(isocitrate dehydrogenase)-->ALPHA-KETOGLUTARATE--(a-ketoglutarate dehydrogenase--NADH MADE)-->SUCCINYL COA--(succinyl coa synthetase--GTP MADE)-->SUCCINATE--(succinate dehydrogenase--FADH MADE)-->FUMARATE--(fumarase)-->L-MALATE--(malate dehydrogenase--NADH MADE)-->OAA!
Can the intermediates in the TCA cycle only be used to make energy?
NO--TCA cycle intermediates can be used for TONS of other processes in the cell.
Is there only one way (as acetyl coa) the carbons can enter the TCA cycle?
NO--carbons enter the TCA cycle at several points.

RXN to know..
PYRUVATE CARBOXYLASE
Converts Pyruvate-->OAA, which can enter TCA!
How the heck is PDH regulated?
When cell needs energy, PDH is active--when cell doesn't need energy, PDH is inhibited.

INHIBITS PDH--NADH, ACETYL COA, PHOSPHORYLATION (by a kinase)

STIMULATES PDH--CALCIUM (because, muscle contraction--need more ATP), INSULIN (high in fed state--need lots of ATP), EPINEPHRINE (need ATP if you're running from a bear), DEPHOSPHORYLATION (by phosphatase)
What is the deal with the PDH kinase/phosphatase?
--Basically, PDH can be regulated by either phosphorylation or dephosophorylation.

--A KINASE PHOSPHORYLATES PDH, INHIBITING it
Kinase--
activated by GLUCAGON, ACETYL COA, NADH
inhibited by pyruvate, NAD, CoA

--A PHOSPHATASE DEPHOSPHORYLATES PDH, ACTIVATING it.
Phosphatase--activated by CALCIUM, EPINEPHRINE, INSULIN.
How is the TCA regulated?
When cell needs energy, TCA is active. When cell does not need energy, TCA is inhibited.

ACTIVATED by--ADP, CALCIUM GDP
INHIBITED by--NADH, ATP, GTP, Succinyl CoA.
What is effect of arsenite in the body?
--Inhibits the DHD subunit of PDH and alpha-KDH (b/c same mechanism as PDH)
--Tx is BAL
What is effect of thymine deficiency?
--TPP is cofactor for PDH.
--No TPP--No PDH activity.
--Lowers activity of PDH and alpha-KDH subunits (b/c same mechanism as PDH)
--Leads to Beri-Beri
What are symptoms of genetic deficiencies in PDH? What do these signify?
1) Lactic acidosis--b/c pyruvate can't become acetyl-Coa--no ETC--only anaerobic glycolysis.
2) Neurological defects--b/c brain needs TCA to make energy--needs to oxidize glucose completely (to CO2, H2O)
Why is giving a ketogenic diet good tx for pt's with deficiencies in PDH?
In other words, the fats can be broken ketogenic--high protein/high fat

-->fats converted into fatty acids and glycerol, which can be used in b-oxidation (makes acetyl coa) and gluconeogenesis (makes glucose)
--> proteins can be broken into a.acids, which can be used in gluconeogenesis (makes glucose).
-->excess acetyl coa is converted into ketones, which the brain can
 use
-->some amino acids will give rise to acetyl coa as well-->can be used to generate energy!
-->more FA-->more b-oxidation in liver-->over time, ketones generated and released (ketogenesis)

-->also, peripheral tissues can use FA's and a.acids