Bch In Musculoskeletal Block

Front 1

PFK-1

Back 1

Second step glycolysis
Rate limiting step
Highly regulated step
uses 1 ATP
Irreversible rxn
Stimulated by AMP
Inhibited by ATP & H+ (anaerobic)

Front 2

HexoKinase

Back 2

step 1 glycolysis
traps glucose (phosphorylates)
uses 1 ATP
Feedback Inhibition - product G-6P

Front 3

G3P - dehydrogenase

Back 3

step 3 glycolysis
maintains NAD/NADH balance
uses 2NADH

Front 4

P Glycerate Kinase

Back 4

step 4 glycolysis
substrate level phosph
Produces +2 ATP

Front 5

Pyruvate kinase

Back 5

step 5
substrate level phosph
Produces +2 ATP
Produces pyruvate (TCA)

Front 6

Lactate Dehydrogenase

Back 6

pyruvate anaerobic becomes lactate using NADH (need NAD for step 3 glycolysis)

Front 7

Phosphocreatine Kinase & Mass Effect

Back 7

based on Log (prod/react) dG
Negative log <1
Positive log >1
ATP->ADP coupled to Cr->PCr

Front 8

Priming phase Glycolysis

Back 8

Uses #2ATP and gets glucose ready

Front 9

Splitting Glucose

Back 9

Produces #4 ATP and provides intermediates for TCA/lactate

Front 10

Transport FA into Mitochondria

Back 10

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

Front 11

Acyl CoA Synthetase

Back 11

activates FA by adding CoA that is removed when attached to carnitine
High E expenditure step

Front 12

Carnitine palmitoyl transferase (CPT)

Back 12

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

Front 13

Carnitne acylcarnitine translocase (CAT)

Back 13

located inner mito and transports

Front 14

Beta Ox Products

Back 14

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

Front 15

Beta Ox steps

Back 15

Remove 2 Carbons from FA
Oxidation - +FADH2
Hydration - -H2O
Oxidation - +NADH
Cleavage - +1 Coa
Repeat

Front 16

Fructose-1,6 BPtase

Back 16

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)

Front 17

Shivering

Back 17

futile cycle of PFK-1 & Fructose-1,6 BPtas.
Net loss 1 ATP
Decouples AMP regulation

Front 18

AMP levels in muscle

Back 18

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

Front 19

H+ on PFK-1

Back 19

build up of lactic acid increases H+ conc and is a feedback inhibitor denoting buildup of glycolysis product

Front 20

Glycogen Futile cycle

Back 20

uses 1 ATP add 1 glycogen but not regenerated upon removel for use
Regulated hormonal Phosphorylation

Front 21

General Phosporylation of enzymes

Back 21

Correlate to fuel mobilization
Starvation, stress, flight response)
Activate fuel use via glycogen & fat
Inactivate fuel synthesis & storage

Front 22

General DePhosphorylation of enzymes

Back 22

Correlate to storage of fuel
(fed state)
Activate synthesis & storage
Deactivate fuel use via glycogen & fat

Front 23

Glycogen Phosphorylase Function

Back 23

breaks down glycogen for use
When P increase activity
Indirectly stim by inc Ca & P the enzyme (2 levels of P)

Front 24

Kinase

Back 24

use P from ATP to P an intermediate or enzyme

Front 25

Epinephrine effect glycogen

Back 25

activates glycogenolysis via GPCR (stim)

Front 26

Forms Glycogen Phosphorylase

Back 26

activated when P (a-form/ relaxed)
Inactive when NO P (b-form/tense)
(stim by AMP)

Front 27

Forms Glycogen Synthetase

Back 27

active when No P (i state)
inactive when P (d state)

Front 28

Insulin effect glycogen enzymes

Back 28

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)

Front 29

Epinephrine effect glycogen enzymes

Back 29

Activates a general protein kinase

1. activates glycogen phosphorylase (glycogen breakdown/ phosphorylated))
2. activates phosphorylase kinase (more phosphorylated form)

Front 30

AMP PFK-1 vs. Glycogen storage

Back 30

AMP stim PFK-1
AMP activates active state of glycogen phosphorylase

Front 31

G-6P mech glycogenolysis

Back 31

inactivates glycogen phosphorylase via allosteric control

Front 32

G-6P mech glycogenesis

Back 32

stimulates glycogenesis by allosteric promotion of glycogen synthetase

G6P overrides hormonal control (epinephrine)

Front 33

Pyruvate Dehydrogenase

Back 33

located matrix mito
Links glycolysis to TCA
aLLOWS ANOTHER 30atp (2 pYRUVATE)
Pyruvate to Acetyl-CoA
3 enzyme complex

Front 34

E1

Back 34

Cofactor - thiamine diP
Category - Prosthetic group
Source - Thiamine

Front 35

E2

Back 35

Cofactor - CoA & Lipoamiode
Category - Co Sub & Prosthetic
Source - Pantothenic acid & N/A

Front 36

E3

Back 36

Cofactor - FAD & NAD
Category - Prosthetic group & Co-Substrate
Source - Riboflavin & Niacin

Front 37

Beri-Beri

Back 37

thiamine deficiency = E1 of PDH not working and loss TCA energy
Weakness & heart failure

Front 38

PDH Regulation types

Back 38

Allosteric & Covalent

Front 39

Allosteric PDH regulation

Back 39

Products of E2/E3
=Acetyl CoA
=NADH
Accumulate
1. slow TCA
2. Beta oxidation
3. High levels NADH

Front 40

PDH & Beta oxidation

Back 40

Beta ox - increases Acetyl-CoA inhibiting PDH

Front 41

Covalent PDH regulation

Back 41

Add P to E1 = inactive
PDH kinase is heavily allosterically activated

Front 42

PDH Kinase

Back 42

deactivated by PDH reactants
-Pyruvate
-CoAS (deacylated CoA)
-NAD+

Front 43

Location PDH

Back 43

this is found inside the mitochondria
Thus the NADH it produces is added to TCA energy