L5 energ prod from carbs 2

Question 1

LO2: princips of regul glycolytic path.

enz catal irrev steps poten sites of contr. eq reacs would still reach eq.

Answer 1

• prod inhib/S unavail- eg NADH inhib G3P to 13BPG.
• allostery- activ/inhib binds outs AS, alt conf. HK inhib by G6P feedb. PFK commit step- in musc inhib by high atp, in liv activ by high insulin. PK activ by high insulin, deP.

Question 2

LO3: expl why lactic ac produc imp in anaer glycol.

Answer 2

• norm NAD re oxid when O ox phos. w/o or mito eg RBC LDH regens. pyruv to lactate.

Question 3

LO4: how blood conc lactate contr.

Answer 3

-to liver and heart. heart conv pyruv to co2. liver to gluc by gluconeogen. imp in liv dis, thiamine defic, alc use NAD to NADH so lactate can tbe used as prod inhib, enz defic.
-RBC, skin, brain , skel musc, GIT prod 40-50g/d norm. stren exercise incl eat 30g/5min. pathol sits eg shock, congest HD.
-plasma conc determ by rates: prod. util liver and heart and musc. dispos kideny.
-hyperlactaemia- 2-5mM below renal thres, no alt blood ph.
-lacic acidosis- over 5mM, above renal thresh, ph decr as buff exceed.
blood conc us less than 1mM.

Question 4

LO5: expl biochem basis of lactose intol and galactosaemia.

Answer 4

-galactose to G1P to G6P in glycol. galac 1P to gluc 1P by galac 1P uridyl transferase, forms UDP galac. UDP galac to up gluc by UDP galac 4’ epimerase.
overall galac +ATP= G6P+ ADP.
UDP gluc acts catalytically.
Galac req for synth gl and prot eg blood grp Ag
-glactosaemia-
GK defic/mut rare= galac accum in tiss, in urine.
transferase defic comm= galac and galac 1P accum PROB:
galac ents other paths eg aldose reductase forms galactitol. in liver. high Km, uses NADH= stuc prot dam by prev maint of free SH= inapp s-s.
how galac 1P affs liv, kidney, brain?
poss rel to sequest Pi prev atp synth.
incr gluc and galactitol in eye incr press can =glaucoma.

Question 5

LO6: expl why PPP imp metab path some tiss.

Answer 5

• G6P to 5C sug Pases by gluc 6P DH. PPP conv them to F6P or G3P. oxidat. prod NADPH for bios when energ high. high NADH=S at top glycol build up, exit glycol to form 5C. imp in liv, adip, RBC.
  no atp prod. loss co2 so irrev. G6P DH contr by NADP/NADPH ratio.
  -funcs- prod cytop NADPH eg for lip synth in liv and adip. maint free SH in RBC.
  prod C3 sug for nt’s so lot in div tiss eg BM.

Question 6

LO7: desc clinic gluc6P DH defic and expl biochem basis of signs and symps.

Answer 6

-defic prevs reduc of NADP+, reduc NADPH. allow inapp s-s. rbc aggreg to Heinz bods, precip as Hb x linked. cause haemolysis=anaemia. also eye lens.
X linked gene defect medit and black US male. pt mut.
also NADPH req to recyc GSH (glutathione tripep) to active reduced form. it protects cells from oxid dam by mop up free rads. RBC partic aff as PPP only source NADPH, and at risk of oxid dam as carrier.
acute haemolytic epis precip by chem that decr NADPH eg antimalarial, sulphonamide, glycosides.

Question 7

pyruv metab.

Answer 7

conv to aCoa by PDH. multienz complex reqs cofacs FAD, thiamine pyroP, lipoic ac. req 4 B vits.
loss co2 irrev. so aCoa cant be conv to gluc.
contr to ensure under cert conds aCoa from b oxid of fa rather then from gluc is used in S3. aCoa allost inhibs PDH. ATP allost inhib and NADH. insulin proms activ by deP.

Question 8

LO1: Key feats glycol.

Answer 8

-FUNCS- oxid gluc/NADH prod. synth 2 atp net. prod c3 and c6 intermeds eg GP, 23BPG.
-FEATS- cytos. exergonic, oxidative. c6 to 2c3 so no co2 loss. with one addit enz can be anaer. irrev.
-imp intermeds- glycerol phosphate from DHAP by G3P DH. in adip and liv, imp to triacylg and Plip synth.
23BPG from 13BPG by BPG mutase. feed out from glycol in RBC. x link pos charges= T state.