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49 Cards in this Set

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Phosphocreatine
in skeletal muscle
uses ATP to store E
Maltose
reducing disacchride of made of 2 glucoses
Lactose
reducing sugar made of glactose and glucose
Sucrose
non-reducing sugar made of glucose and fructose
law of mass action
Vmax is proportional to collisons btwn reactants
Competitive Inhibitor
I binds to E
I inc apparent Km
Vmax is unaffected
Non-Competive Inhibitor
binds E and ES
Vmax is decreased
Km can remain unchanged
Uncompetitive Inhibitor
I binds to ES
apparent Km dec
Vmax dec
GLUT 1 & GLUT 3
basal glucose uptake
Km = 1
all cells
GLUT 2
live and B-cells
Km = 15-20
glu uptake prop [blood glu]
inc glu uptake = inc insulin = carb storage
GLUT 4
Km = 5
skeletal muscle & fat cells
insulin inc = translocation to plasma memb
GLUT 5
fructose uptake in small intestine
SGLT 1
sodium glucose cotransporter
small intestine
glucose & galactose uptake
Hexokinase
low Km
use Mg-ATP
inhibited by product inhibitied by G6P
Glucokinase
liver and pancreatic b-cells
higher Km
not inhibited by G6P
Glycogen Phosphorylase
cleaves alpha 1-4 bonds
non-reducing ends >4 from branch
uses PLP
releases G1P
Phospholucomutase
G1P --> G6P
Glucose-6-phosphotase
in liver, hydrolyzes G-6-P to glucose
debranching enzyme
transfers block of 3 glu from a-1,6 branch to diff a-1,4 AND hydrolyzes the remaining a-1,6 glucose unit
releases 1 free glucose
UDP-glucose pyrophosphorylase
rxn is readily reversible driven by hydrolysis of pyrophosphate
pyrophosphatase
hydrolyzes pyrophosphate PPi
Glycogen Synthase
catalyzes the elongation of non-reducing termini of glycogen forming a-1,4 linkages
nucleoside diphosphate kinase
UDP --> UTP
readily reversible Km ~1
Glycogenin
tyrosine dimer
Branching enzyme
7 glu residues to a 6 position on a nearby chain
Factors that increase glycogen breakdown
epinephrine, glucagon, AMP, Ca++
Factors that decrease glycogen synthesis
insulin, ATP, G-6-P, glucose (liver)
Glycogen Phosphoylase
dimer
T-state = inactive
R-state = active
a - phosphorylated - active
b-not phos - inactive
Phosphorylase Kinase
phos glycogen phosphorylase a
activated by Ca & PKA phos
Phosphoprotein phosphatase 1
PP1
dephos glycogen phosphorylase
inactivated by PKA P of I
activated by insulin TRK P of R
Phosphofructose Kinase
activators?
Inhibitors?
ATP, Citrate, dec pH - feedback inhib changes Km
AMP, ADP, Pi - allosteric activators that compete w/ ATP for binding site
F26BP => activator
Fructose 2,6 Bisphosphate
made by PFK2 + ATP
degraded by FBPase 2
Phosphofructokinase 2
makes F26BP and is stimulated by insulin activation of phosphoprotien phosphotase
Fructose bisphosphatase 2
breaks F26BP -> F6P
Activated by glucagon activation of cAMP dependent PKs
Aldolase
(glycolysis) uses Schiff base
Triosephoasphate isomerase (TIM)
ketose -> aldose
driven by removal of GAP
(glycolysis)
Glyceraldehyde-3-phosphate dehydrogenase
(glycolysis)
ox-red
makes NADH
makes high E phosphate bond (mixed anhydride)
inactivated by heavy metals (arsenate)
Phosphoglycerate Kinase
(glycolysis)
substrate level phosphorylation -> ATP
Phosphoglycerate Mutase
(glycolysis)
shifts Phos from C3 to C2
Enolase
(glycolysis)
dehydration creating high E posphoenol bond
driven by entropy (H2O loss)
Pyruvate Kinase
(glycolysis)
substrate level phosphorlyation -> ATP
Pyruvate Kinase Regulation
feedforward activation by F16BP
feedback inhibition by ATP & alanine
inactivated by phos by cAMP PKs
Enzymes Required for Fructose to enter glycolysis (3)
fructokinase
fructose 1 phospate aldolase
triose kinase
Enzymes Required for Glactose to enter glycolysis (3)
galactose kinase
gal-1-phos uridyl transferase
UDP gal 4 epimerase -> UDP glu
Effects of insulin on glycolysis?
glycagon?
insulin - stimulates
glucagon - inhibits
Pyruvate Carboxylase
allosterically regulated biotin dependent enzyme -> OAA
PEP carboykinase
decarboylates OAA -> PEP at expense of GTP
Fructose-1,6-Bisphosphatase
F-16-BP -> F6P
inhibited by AMP
activated by ATP
Glucose-6-phosphatase (G6Pase)
G6P -> Glu
rich in liver but absent in muscle
luminal side of ER facilitated by memb transporters in ER memb