Under what conditions is D-glucose converted to lactic acid?

and how many?

what enzyme?

anaerobic

2

LDH

synthesis of glucose from non-carb precursors

rxns by-pass exergonic rxns

brain uses what under non starvation conditions,

under starvation conditions?

1 Glucose

2 ketone bodies

Glucose

erythrocytes can only produce 2 atp

how much glucose does body require per day,

how much of that does brain req

160g

120 g

investment of 2 atp

phosphorylation of glucose

Neg charge sequesters glucose within cell and makes it less stable

RXN1

GLUK->G6P

Specifics

1 atp invested

irreversible

enzyme: hk I-III =mg dep

in liver gk=hkIV

gk: not inhibited by g6p nor is easily sat like hk

when is hk saturated?

gk?

1) at normal blood gluc levels

2) after glucose rich meals

what other sugars can hk phosphorylate?

gk?

1) fructose, mannose, and
glucosamine,

2) none

enzyme: phosogluco isomerase

Opening of the ring and recycliztion as a 5 membered ring

Mg dep

reversible

aldose to ketose

pfk-1 ATP dep

irreversible

committed step most important step

Aldolase

2nd stage

reverse aldol condensation

DHAP-> ga3p

where does equilibrium lie?

triose phosphate isomerase rxn

equilibrium is to the the left on dhap.

triose phosphate isomerase is kinetically perfect

GA3P DH

addition of inorganic phosphate and REDUCTION of NAD+ to NADH

can uncouple substarte level phosporylation

it inhibits e2 of pdh ocmplex which is link btwn glycolysis and tca. mimics sulfur

effects of 2,3 bpg

how is it made and how does it convert back to glycolytic interm

- allosteric effector of 02 release from hg. incr release of o2 in tissue

b) bisphosphoglycerate mutase

2,3 bisphosphoglycerate phosphatase

PG Kinase

substrate level phosphorylation

transfer of 1 phosphate 1 adp to form ATP

Remeber 2 per glucose molecule

NAD + is reduced

PG MUTASE

imporant becasue 3-pg cannot be dehydrated

enolase

inhibited by flourine

Pyruvate Kinase

2nd substrate level phos

NAD + consumed in the GA3p DH is recycled in the LDh

NADH which was produced in same rxn is comsumed by LDH, there by recycling

steps in ethanol metabolism

ethanol to acetaldhyde via alcohol DH

Acetaldhyde to acetate via acetaldhyde DH

NADH/NAD+ ratio is increased.

remember NAD+ is needed at GA3 DH step

increase in FA synethesis and

glycerol 3 phosphate --> Fatty liver

favors ketosis= ketone bodies

accumulation of acetaldehyde=toxic

TCA activity is depressed

FA ox is depressed

8/1

1/1

in asians 40% have an isozyme which has a high km for acetaldhye (Toxic)

Automatic protection from alcoholism

Hexokinase

pfk-1

pk

hk

pfk-1

pk

what down regulated pk activity?

upregulates?

alanine and cAMP dep phosphorylation

b)f 1,6 bp

how many allosteric binding sites are on pfk-1

how many substrate binding sites?

a)4

b) 2

high insulin to glucon ration.

stimulates the kinase activity of pfk-2 via protein phosphorylase

phosphorylase removes phosphate from pfk-2

Glucogon or epinepherine

low insulin to glucogon ration which leads to phosphorylation of pfk-2 (via inc cAMP-> inc pka) via up regulation of  fructose 2,6 bisphoshatase activity

in LIVER

Epinephrine effects on pfk-2 in a) liver

b) cardiac muscle

c) what are these enzymes in relation to each other?

a)elevates cAMP -> inc in phosphatase activity->less f 2,6 bp

liver phosphorylation incr phosphatase activity

B) incr in cAMP will increase kinase acitvity and more f 2,6 bp is made

 cardiac phosphorylation incr kinase activity

c) isozymes

what are the 2 forms of pyruvate kinase?

what are similarities 3?

l form is inhibited by low blood glucose = incr glucogon and incr cAMP dep phosphorylation

l form will not consume gluc when its more urgently needed by brain and muscle

pfk-1 and pk

serine residues are being phosphorylated

fruc 1,6 bisphosphatase is main step. it convert f 1,6, bp -> f 6p

 up regulated by citrate down reg by amp and f 2,6 bp  opp of pfk-1

reduced mitochondrial atp production --> activates pfk1 which stimulates glycolysis --> incresased lactate prod

can lead to shock and resp disorders