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43 Cards in this Set

  • Front
  • Back
Second step glycolysis
Rate limiting step
Highly regulated step
uses 1 ATP
Irreversible rxn
Stimulated by AMP
Inhibited by ATP & H+ (anaerobic)
step 1 glycolysis
traps glucose (phosphorylates)
uses 1 ATP
Feedback Inhibition - product G-6P
G3P - dehydrogenase
step 3 glycolysis
maintains NAD/NADH balance
uses 2NADH
P Glycerate Kinase
step 4 glycolysis
substrate level phosph
Produces +2 ATP
Pyruvate kinase
step 5
substrate level phosph
Produces +2 ATP
Produces pyruvate (TCA)
Lactate Dehydrogenase
pyruvate anaerobic becomes lactate using NADH (need NAD for step 3 glycolysis)
Phosphocreatine Kinase & Mass Effect
based on Log (prod/react) dG
Negative log <1
Positive log >1
ATP->ADP coupled to Cr->PCr
Priming phase Glycolysis
Uses #2ATP and gets glucose ready
Splitting Glucose
Produces #4 ATP and provides intermediates for TCA/lactate
Transport FA into Mitochondria
Binding Protein removes FA from blood/albumin
Activate FA -> Palmitoyl-CoA
Attached to Carnitine for transport
Detached from transport as Palmitoyl
CoA does NOT cross transporter
Acyl CoA Synthetase
activates FA by adding CoA that is removed when attached to carnitine
High E expenditure step
Carnitine palmitoyl transferase (CPT)
located outer mito membrane
Uses E from CoA to attach to carnitine
Deficiencies lead to muscle weakness

Located inside mito to reactivate FA by adding CoA
Carnitne acylcarnitine translocase (CAT)
located inner mito and transports
Beta Ox Products
1 cycle uses #2C
1 Acetyl CoA / #2 carbons in FA
(#C/2) - 1 is # cycles
1FADH2 & NADH per cycle
use 1 H2O per cycle
Beta Ox steps
Remove 2 Carbons from FA
Oxidation - +FADH2
Hydration - -H2O
Oxidation - +NADH
Cleavage - +1 Coa
Fructose-1,6 BPtase
reversible version PFK-1
allows post anaerobic replenish of glycogen from lactate
Does NOT replenish ATP and thus produces futile cycle
Inhibit - AMP (low E state)
futile cycle of PFK-1 & Fructose-1,6 BPtas.
Net loss 1 ATP
Decouples AMP regulation
AMP levels in muscle
AMP levels are much lower and thus more sensitive to small increases (compared to ATP)
This allows large amounts ATP but sensitive regulation via AMP
Stimulates Glycolysis & Glycogenolysis
H+ on PFK-1
build up of lactic acid increases H+ conc and is a feedback inhibitor denoting buildup of glycolysis product
Glycogen Futile cycle
uses 1 ATP add 1 glycogen but not regenerated upon removel for use
Regulated hormonal Phosphorylation
General Phosporylation of enzymes
Correlate to fuel mobilization
Starvation, stress, flight response)
Activate fuel use via glycogen & fat
Inactivate fuel synthesis & storage
General DePhosphorylation of enzymes
Correlate to storage of fuel
(fed state)
Activate synthesis & storage
Deactivate fuel use via glycogen & fat
Glycogen Phosphorylase Function
breaks down glycogen for use
When P increase activity
Indirectly stim by inc Ca & P the enzyme (2 levels of P)
use P from ATP to P an intermediate or enzyme
Epinephrine effect glycogen
activates glycogenolysis via GPCR (stim)
Forms Glycogen Phosphorylase
activated when P (a-form/ relaxed)
Inactive when NO P (b-form/tense)
(stim by AMP)
Forms Glycogen Synthetase
active when No P (i state)
inactive when P (d state)
Insulin effect glycogen enzymes
Activates a general protein phosphatase

1. inactivates glycogen phosphorylase (blocks glycogen breakdown/ dephosphorylated))
2. inactivates phosphorylase kinase (more dephosphorylated form)
3. Decrease cAMP 2nd messenger (activates phosphodiesterase)
Epinephrine effect glycogen enzymes
Activates a general protein kinase

1. activates glycogen phosphorylase (glycogen breakdown/ phosphorylated))
2. activates phosphorylase kinase (more phosphorylated form)
AMP PFK-1 vs. Glycogen storage
AMP stim PFK-1
AMP activates active state of glycogen phosphorylase
G-6P mech glycogenolysis
inactivates glycogen phosphorylase via allosteric control
G-6P mech glycogenesis
stimulates glycogenesis by allosteric promotion of glycogen synthetase

G6P overrides hormonal control (epinephrine)
Pyruvate Dehydrogenase
located matrix mito
Links glycolysis to TCA
Pyruvate to Acetyl-CoA
3 enzyme complex
Cofactor - thiamine diP
Category - Prosthetic group
Source - Thiamine
Cofactor - CoA & Lipoamiode
Category - Co Sub & Prosthetic
Source - Pantothenic acid & N/A
Cofactor - FAD & NAD
Category - Prosthetic group & Co-Substrate
Source - Riboflavin & Niacin
thiamine deficiency = E1 of PDH not working and loss TCA energy
Weakness & heart failure
PDH Regulation types
Allosteric & Covalent
Allosteric PDH regulation
Products of E2/E3
=Acetyl CoA
1. slow TCA
2. Beta oxidation
3. High levels NADH
PDH & Beta oxidation
Beta ox - increases Acetyl-CoA inhibiting PDH
Covalent PDH regulation
Add P to E1 = inactive
PDH kinase is heavily allosterically activated
PDH Kinase
deactivated by PDH reactants
-CoAS (deacylated CoA)
Location PDH
this is found inside the mitochondria
Thus the NADH it produces is added to TCA energy