Cori cycle:

(Intramuscular) Glycogen -> GLC -> Pyruvate ---------> Lactase

NAD+->NADH NADH->NAD+

(Liver) Lactate ---(LDH)-- Pyruvate ->->-> GLC

NAD+ -> NADH

Transamination:

Alananine + Oxaloacetate ----(Alanine Transaminase)----- Pyruvate + Aspartate

Aspartate --- Oxaloacetate -- Glucose

Glutamate -- Alpha Ketoglutarate -- Oxaloacetate -- Glucose

Alanine comes from protein degradation during severe starvation

Pentose Phosphate Pathway (Hexose Monophosphate Shunt)

Occurs mainly in liver + Adipose tissue Creates NADPH (reducing agent) + Ribose

Two stages: Oxidative + Non Oxidative Occurs in rapidly dividing cells

If a cell needs NADPH+ Ribose; PPP stops at the oxidative stage

If a cell only needs NADPH, PPP fully proceeds to generate intermediate + NADPH.

Intermediate is then used for energy

High Blood Glucose levels -> stimulates Glycolysis + PPP

Xylulose-5-P is a metabolic regulate

Xylulose-5-P => Protein Phosphatase2; which will dephosphorylate PFK-2 / Fructose-2,6-BisPhosphate

Its a bifunctional enzyme that can turn PFK-2 activity on

PFK-2 synthesizes Frc-2,6-BisP which allosterically activates PFK-1, initiating Glycolysis

Xylulose-5-P activates ChREBP (Carb responsive elemental binding protein); which stimulates lipid
synthesis

Glycogen: GLC polymer attached in (alpha 1-4) bonds with branches in (alpha 1-6) links

Starch can be Amylose or Amylopectin

Alpha-Amylase (salivary/pancreatic) B-Amylase (plants)

a-Amylase => Endoglycosidase

B-Amylase => Exoglycosidase

Starch becomes compact with numerous branches when amylase acts on it; called limit dextrin

the polysaccharide fragments remaining at the end (limit) of exhaustive hydrolysis of

amylopectin or glycogen by a-1,4-glucan maltohydrolase or -amylase, which cannot hydrolyze
the a-1,6 bonds at branch points; accumulates in individuals with type III glycogen storage
disease.

Aerobic Respiration:
Glycolysis (occurs in cytosol)
Glucose (6c) => 2 (3c) pyruvate + 2 ATP + 2 NADH
2 Pyruvate => 2 Acetyl CoA (2c) + 2 NADH (occurs in mitochondria)
TCA (occurs in mitochondrial matrix)
Acetyl CoA (2c) => 2 CO2 + 3 NADH + [FADH] + GTP
(per glucose: 6 NADH + 2 FADH2 + 2 GTP)

ETP (oxidative phosphorylation)

NADH/FADH2 -> ATP (occurs in mitochondrial membrane)
CoEnzyme A + Sulhydral group = CoASH
Pyruvate + CoASH + NAD+ ----->>>> acetyl CoA + NADH + H+

Pyruvate Dehydrogenase Complex breaks into 3

E1 = Pyruvate Dehydrogenase ----->>>>> TPP as Prosthetic group
E2 = Dihydrolipoamide acetyl transferase (transacetylase) ----->>>>> lipoamide as prosthetic
group
E3 = Dihydrolipoamide dehydrogenase ---->>>>> FAD as prosthetic group

PDC requires 5 coenzymes

CoASH NAD+ (both are cosubstrates, no need to regen them)
Thiamine pyrophosphate (TPP) lipoamide FAD
^ (prosthetic groups / tightly bound must regen)
NAD+ carries 2 e- in the form of H= (hydride) [NAD can accept/donate 2 e- simultaneously]
FAD can accept/donate 1 or 2 e- at a time

Coenzyme A fxns: Activation of acyl groups for transfer via nucleophilic attack
And activation of a-hydrogen of acyl group for abstraction
The Sulfhydral group on CoA forms thioester linkages w/ acyl groups

Lipoic acid fxns to couple acyl-group transfer and e- transfer during oxidation + decarboxylation
of a-keto acids. Its found in pyruvate dehydrogenase + a-ketoglutarate dehydrogenase.
Lipoic acid covalently binds to enzymes via amide bond w/ NH2 of a lysine side chain
This type of cleavage occurs in Frc-BisP aldolase rxn w/
glycolysis; but cannot occur in acetate because it lacks
a beta carbon
 This occurs in transaldolase rxn; but requires
hydroxylation of acetate (which is not favorable for
acetate)

Citrate is a symmetrical molecule that reacts

asymmetrically w/ citrate synthase generating only 1
stereoisomer. (Considered prochiral)

TCA cycle is regulated with 3 reactions:

Citrate synthesis: (-) ATP (-) NADH
(-) Succinyl CoA
Isocitrate dehydrogenase (-) NADH (-) ATP
(+) ADP
a-Ketoglutarate dehydrogenase (-) NADH (-)
Succinyl CoA (+) AMP

The dehydrogenase complex is negatively

inhibited by
Acetyl CoA NADH ATP
Positively by NAD+ CoASH

Covalent modification (phosphorylation)

inactivates PDC: Pyruvate
Dehydrogenase Complex

Fluoroacetate (toxin) blocks the TCA cycle b/c Aconitase is inhibited by fluorocitrate; which is
formed by fluoroacetate

TCA is amphibolic: Anabolic + Catabolic (divided into two steps)

Catabolic: Isocitrate dehydrogenase + a-ketoglutarate dehydrogenase
Anabolic:
Oxaloacetate --------->>>>>> Glucose
Oxaloacetate --------->>>>>> Aspartate -> Proteins
a-Ketoglutarate ------>>>>>> Glutamate -> Proteins
Succinyl CoA ------->>>>>> Porphyrins -> Heme
Citrate ------>>>>>>> Acetyl CoA + Oxaloacetate
^ -->>> Fatty acid synthesis

Anaplerotic (filling up) reactions provide

intermediates for the TCA cycle
Ex: Pyruvate + CO2 ------(pyruvate
carboxylase)------>>>> Oxaloacetate
Pyruvate Carboxylase + (PEP)
Phosphoenolpyruvate carboxylase +
Malic enzyme catalyze the anaplerotic
reactions, which replenish TCA
intermediates