BIOC C

the sum of chemical transformations

metabolism= anabolism + catabolism

metabolism

degrade biomolecules carb/fat/protein → CO2 H2O and NH3

byproducts- ATP, NADPH, NAHD2, FADH

catabolism=

make biomolecules using sugar, AA, FA, nitogenous bases

byproducts- ADP, HPO2-,NAD+,FAD,NADP+

anabolism=

exergonic (release a lot of energy

rate limiting steps are ____(ender or exergonic)

acetyl coa, macromolecules

catabolism coverges to_____, anabolism diverges to ____________

F, rate limiting steps are far form equalibrium witha lot of [S] and low [P]

rate limiting steps are near equalibrium (T/F)

substrate

in most steps enzyme is in excess and it waits for more substrate, but in rate limiting steps ____ can be in excess and pathway is still slowed

glucose→ glucose 6 phosphate

fructose 6 phosphate → fructose 1,6 bisphosphate

phosphenolpyruvate→ pyruvate

what are the three exegonic steps of glycolysis

hexokinase atp→adp

phosphofuctokinase-1 atp→adp

pyruvate kinase 2adp→2atp

what enzymes for these three glycolysis steps

glucose→ glucose 6 phosphate

fructose 6 phosphate → fructose 1,6 bisphosphate

phosphenolpyruvate→ pyruvate

energy available to work in a system

gibbs free energy

negative

a reaction is spontaneous when deltaG is ____

greater

spontaneous when substrate has ______ energy than products

increase stability, lower energy, more entropy, energy released powers cell

why is -deltaG more favourable

coupling spontaneous with nonspontaneous (ex. hydrolyze ATP)

how do +deltaG rxn occur in cell if not spontanous

deltaG<0 spontaneous (exergonic)

deltaG>0 nonspontanous (endergonic)

deltaG=0 at equilibrium

deltaG<0

deltaG>0

deltaG=0

negative

the deltaG of the three rate limiting rxns of glycolysis is very ______

decrease

coupling ATP to a reaction _______ the deltaG (increase or decrease)

lowers Ea

hexokinase _______________ so that ATP hydrolysis and glucose phosphorylation occur simutaneously

deltaG=deltaG’+RTln [P]/[S]

deltaG=

negative (low product, high reactant concentration)

in deltaG equation

ln small/large number gives a ______ deltaG

maximum, glucose-6-phosphate

muscle hexokinase-1 is normally at ______ activity but it is allosterically inhibited its product _____

lower, fructose-6-phosphate

liver hexokinase-IV (glucokinase) is normally not at max activity as it has a _______ glucose affinity and is inhibited further by _______

lower

hexokinase-1 K0.5=5

glucokinase K0.5=10

hexokinase-1 has a _______ K0.5 than glucokinase (hexokinase-IV)

when glucose concentration increases

when does glucokinase activity increase?

inactive, active

where is hexokinase-IV in the nucleus is ________ hexokinase-IV in the cytoplasm is _______

high fructose-6-phosphate

what triggers hexokinase-IV to move cytoplasm→ nucleus

repress- ATP, citrate

activate- ADP, AMP, F2,6BP (fructose 2,6- bisphosphate)

explain the allostery for PFK-1 (phosphofructokinase-1) (what inhibits/ activates)

substrate and inhibitor

ATP for PFK-1 acts as a _______ and ________

inhibit- ATP, long chain fatty acids, acetyl-coa, alanine

activate-F-1,6-BP

inhibitors and activators of PK (pyruvate kinase)

glucagon (increased cAMP) and PKA enzyme, insulin and PP enzyme

PK is deactivated by ______ signal and activated by _________

phosphorylated

when PK is inactive it is ________

glycolysis, gluconeogenesis

when PK is active ______ is favoured and _____ is repressed

glycolysis, gluconeogenesis

so insulin signals for _________ to occur and glucagon signals for _________ to occur

liver

where does PK regulation take place?

to resynthesize glucose to keep the body functioning (resynthesise from lactic acid built up in exercise for ex.)

why is gluconeogenesis important?

10,8,1

step 1, 3, 10 glycolysis = step ____, _____, ______ gluconeogenesis

pyruvate to phospenolpyruvate

step 1 gluoneogenesis converts ________ to __________

pyruvate enters mitochondria*

pyruvate carboxylase: pyruvate+ CO2→ oxaloacetate

mitochondrial malate dehydrogenase: oxaloacetate + NADH→malate + NAD+

malate exits mitochondria*

cytosolic malate dehydrogenase: malate + NAD+ →oxaloacetate + NADH

cytosolic PEP carboylase: oxaloacetate → PEP +CO2

describe the pathway from pyruvate to PEP

the malate helps facilitate NADH movement form mitochondria to cytoplasm

what is the point of doing oxaloacetate→ malate→ oxaloacetate?

when lactate feeds glucoeogenesis, LDH produces cytosolic NADH so liver PEP carboxylase produces PEP directly

when does this process not go through the mitochondria?

fructose-6-phosphate-→ fructose-1,6-bisphosphate (enzyme: fructose1,6 bisphosphatase-1)

step 8 gluconeogenesis

glycolysis, it inhibits gluconeogenesis

does F26-BP increase rate of glycolysis or gluconeogenesis?

100x increse

10x decrease

by what factor does F26-BP increase rate of glycolysis?

what factor does it inhibit gluconeogensis?

by PFK2 and FBPase-2 (two subunits of the same enzyme)

how is F26BP regulated?

PKA2 (encourages higher production of F26BP which activates glycolysis)

insulin encourages glycolysis, which half of the bi functional PFK2/FBPase2 enzyme does it activate? LIVER

FBPase2 (causes F26BP to decrease which favours gluconeogenesis)

glucagon (increase cAMP) encourages gluconeogenesis, which half of bi functional PFK2/FBPase2 enzyme does it activate? LIVER

phosphorylation activates PFK2 instead (the oppisite) as the heart isoform always wants to be doing glycolysis

how is the heart or other muscles regulation different than the liver?

glucagon, reduces

PKA phosphorylates bifunctional enzyme in response to ______ activating FBPase2, this _______ F26BP production

insulin, increases

PP dephosphorylates bifunctional enzyme in response to ________ activating PFK2, this _______ F26BP production

PFK2 and glycolysis

xyulose 5 phosphate from the pentose phosphate pathway allosterically upregulates PP and therefore promotes ________________

T

even when liver does gluconeogenesis, heart still does glycolysis (T/F)

Ser32

Ser406

liver isozyme phosphorylation on _______ activates FBPase2

cardiac phosphorylation of ____ and ______ activates PFK2

F6P→ F16BP

what is the first commited step in glycolysis?

they signal abundant energy so no need to speed up glycolysis

why do ATP, acetyl coa, long chain FAs, alanine all inhibit PK

low, slows (reserve sugar for organs that need it)

glucagon signals _______ blood sugar (low/high) and ________ (slows/speeds up) liver PK

inhibits- citrate, ATP

activates- F26BP, AMP, ADP

PFK1 (for glycolysis) what inhibits and activates

inhibits- F26BP, AMP

FBPase1

glycolysis, gluconeogenesis

higher energy moleules signal ________ to occur and lower energy molecules signal ________ to occur

gluconeogenesis

low energy molecules inhibit ________

insulin→ active PFK2 (enzyme:phosphoprotein phosphatase)

active PFK2 enzyme F6P→F2,6BP

encourages glycolysis (block gluconeogenesis)

explain what happens when insulin is a signal

glucagon (increased cAMP) → active FBPase2 (emzyme: PKA)

active FBPase2 enzyme catalyses F2,6BP→F6P

encourages gluconeogenesis (block glycolysis)

explain what happens when glucagon is a signal

a pathway that runs parallel to glycolysis, main job to make NADH and ribulose (for nucleotides), relates to glycolysis as it starts with glucose-6-phosphate

what is the pentose phosphate pathway?

G6P oxidation produces 2NADPH and ribulose5P

explain the oxidative phase of the PPP, reactants and products

replenishes the G6P and glycotic intermediates and is a source of xyulose6P

explain teh PPP non oxidative phase