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24 Cards in this Set

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What is the PPP?
AKA: "Hexose monophosphate shunt"

Used to:
1) make NADPH for reductive biosynthesis as an anti-oxidant
2) produce RIBOSE-5-PHOSPHATE to make nucleotides!
What pathways require NADPH?
(produced by PPP)

NADPH used to make:
1) FAs
2) Cholestrol
3) Neurotransmitters
4) Nucleotides

Also, REALLY important in detox--
1) Reduction of glutathione
2) Cytochrome p450 monooxygenase
What tissues use the PPP?

testes, adipose, ovary, mammary gland, RBC's
What are the steps in the PPP?

(well, the ones we need to know)
G-6-P--(G-6-PDH-makes NADPH)-->6-PHOSPHOGLUCONO-LACTONE--(lactonase)--6-PHOSPHOGLUCONATE--(6-phosphogluconateDH--makes NADPH)-->RIBULOSE-5-P

-->after this step, there are TONS of reactions using carbon intermediates-->end up generating F-6-P and G-3-P-->GLYCOLYSIS

-->So, overall, w/PPP, you generate RIBOSE-5-P (nucleotide synthesis) and GLYCOLYTIC INTERMEDIATES--nothing is wasted!
How are the PPP enzymes regulated?
-->catalyzes rate limiting step
-->ACTIVATED by..insulin

Both of these reactions produce NADPH-->makes sense-->when insulin is HIGH, you want to make sure you have enough reducing power to catalyze FA (and sterol) synthesis!
What is G-6-PDH deficiency?
-->Oxidations in your body generate tons of peroxide compounds (H202, RO-OH)-->generate OH radicals-->damage tissue.
-->catalase and GLUTATHIONE PEROXIDASE neutralize these compounds...

(glutathione peroxidase rxn)

**So, glutathione is OXIDIZED in the reaction and needs to be regenerated to continue neutralizing compounds.

-->GLUTATHIONE REDUCTASE uses NADPH to reduce/regenerate glutathione for another neutralizing rxn...

(glutathione reductase rxn)

-->G-6-PDH generates NADPH during the PPP.
-->No G-6-PDH=NO NADPH=No glutathione reductase rxn=NO regenerated glutathione!
-->leads to: increased OH free radicals and tissue damage.
-->Also, damages RBC's-->causes hemolytic anemia!
Why is G-6-PDH sometimes not so bad?
-->G-6-PDH leads to increased presence of toxic OH compounds in the cell.
-->damage tissue but also CONFER RESISTANCE to malaria (odd..)
What is beri beri?
-->THIAMINE deficiency
-->Transketolase (used in PPP) uses TPP as a cofactor.
-->TPP can't work w/no thiamine-->no PPP!
What is gluconeogenesis?
-->synthesis of glucose from non-carb precursors
-->produces glucose that can be released into blood during times of low glucose (overnight fast, high protein/fat diets, exercise).
-->glucose used by:
-Brain (only glucose can cross BBB)**
-RBC (entirely dependent)**
-muscle (during exercise a little)

**=tissues that can't use FA's generated by b-oxidation during fasting.
In gluconeogenesis increased or decreased in diabetics?
WAY increased-->why they have such ridiculous hyperglycemia!

--Don't have any insulin--never gets turned off!
What are the steps in gluconeogenesis?
PYRUVATE--(**pyruvate carboxylase)-->OAA--(**PEPCK)-->PEP--(**enolase)-->2-PHOSPHOGLYCERATE--(phosphoglycerate mutase)-->3-PHOSPHOGLYCERATE--(phosphoglycerate kinase)-->1,3 BISPHOSPHOGLYCERATE--(G-3-PDH)-->G-3-P

G-3-P--(triose phosphate isomerase)-->DHAP

G-3-P+DHAP--(aldolase)-->F-1,6-bisP--(**F-1,6-bisPase)-->F-6-P--(phosphoglucose isomerase)-->G-6-P--(**G-6-Pase)-->GLUCOSE

**--different than glycolysis enzymes
What are the precursors to gluconeo?
Where do they enter the pathyway?
1) Lactate
2) Glycerol
3) A.Acids (Alanine)

Glycerol (from TAG hydrolysis)-->DHAP
A.Acids-->Pyruvate, OAA
If the pyruvate kinase step (glycolysis) is irreversible, how the heck does Pyruvate-->PEP in gluconeogenesis?
-->It uses TWO enzymes

Pyruvate Carboxylase


Pyruvate carboxylase-->needs ATP
PEPCK-->needs GTP
-->Both rxns require energy (generated from b-oxidation)

-->In addition, pyruvate carboxylase is a BIOTIN requiring enzyme.

PC binds biotin-->Biotin binds lysine-->lysine+biotin bind CO2

**CO2 will NOT bind biotin unless Acetyl CoA is present (generated from B-oxidation)--IMPORTANT
Why is liver the only tissue that can really do gluconesis?
-->It has G-6-Pase!

-->Muscle and other non-gluconeogenic tissues lack this enzyme-->cannot release free glucose.
Describe compartmentalization of gluconeogenic generation of OAA
PYRUVATE CARBOXYLASE reaction (Pyruvate-->OAA) occurs in the mitochondria.

-->After being made, OAA needs to get into the cytosol where the other gluconeo enzymes are located--> can not cross the mitochondrial membrane to undergo the rest of gluconeogenesis.
-->Must be converted to malate-->shuttled out of mitochondria-->converted into OAA+NADH-->ready for PEPCK reaction!

**OAA can also be converted to aspartate and pushed across membrane.

However, not ALWAYS the case..
-->In humans, there is sometimes a mitochondrial PEPCK, which generates OAA-->PEP in one step, circumventing the need for the OAA shuttling.
Describe compartmentalization of G-6-Pase.
-->G-6-Pase is located in the ER.
-->several possible reasons:

1) isolate it--prevent competing reactions
2) release glucose in "packets"
Describe hormonal regulation of gluconeogenesis
G-6-Pase and PEPCK

ACTIVATED by..glucagon, epinephrine, cortisol
INHIBITED by..insulin
Describe PEPCK promotor
-->PEPCK is an INDUCIBLE enzyme.
-->contains cis-acting elements that bind CREB and GRE-->ACTIVATE transcription of more PEPCK
-->bind IRE-->inhibit PEPCK transcription.
-->IRE is insulin-regulated transcription factor-->will INHIBIT PEPCK transcription when high
-->So, when insulin is low, PEPCK can be made!
From BRS--"Transcription of gene encoding PEPCK is stimulated by binding of proteins phosphorylated by cAMP and glucocoritcoid-protein complexes" (CREB?)
Describe allosteric regulation of gluconeogenesis (compared to glycolysis)

ACTIVATED by..Acetyl CoA


F-1,6-BisPase (F-1,6-BisP-->F-6-P)
INHIBITED by..AMP, F-2,6-BisP (hormonal control)
Describe the Cori Cycle
RBC-->release lactate
Muscle-->releases lactate and pyruvate

-->pyruvate/lactate can go to liver for gluconeogenesis
-->Where does resulting glucose go? mainly, to RBC-->Low insulin means low glut-4 transporters in muscle, so less glucose can get in.
Why is the muscle releasing pyruvate/lactate during fasting/exercise?
-->There is too much pyruvate present. Supply of pyruvate from glycolysis OUTSTRIPS the muscle's ability to use it! (in TCA; etc)
--Also, PDH (pyruvate-->acetyl coa) may be inhibited due to INCREASED acetyl coa from b-oxidation.
--As exercise is prolonged, we burn more fat and less glucose-->b/c elevated citrate inhibits PFK-1-->increased G-6-P-->inhibited hexokinase
Describe the Alanine cycle.
-->Alanine released (derived from proteolysis and pyruvate) from muscle-->travels to liver for gluconeogenesis
-->Liver makes glucose that really isn't used by muscles--used by "needier" tissues--RBC's, brain--muscle uses B-oxidation and ketones.
What are some deficiencies/diseases in gluconeogenesis?
1) G-6-Pase deficiency
-->get lactic acidosis, fatal hypoglycemia.

2) F-1,6-BisPase deficiency
-->get lactic acidosis, fatal hypoglycemia1
Describe effects of ethanol (booze) ingestion on gluconeogenesis
-->Catalyzes following rxn:

Ethanol + NAD-->Acetaldehyde+NADH

-->acetaldehyde damages the liver.
-->Increased NADH inhibits TCA cycle, b-oxidation and activates lipogenesis
-->increased NADH favors lactate production-->lactate is shunted into alternative rxn pathway-->not available as gluconeo precursor-->less gluconeogenesis.
-->decreased b-oxidation=decreased acetyl coa-->can't activate pyruvate carboxylase-->less gluconeogenesis from pyruvate
-->get lactic acidosis and hypoglycemia
Shows links b/w b-oxidation and gluconeo:

b-oxidation makes NADH-->stimulates pyruvate carboxylase->stimulates gluconeo

NAD-->stimulates b-oxidation and TCA cycle-->makes energy