Ackerman Lectures 9-10 Flashcards Preview

Biochem Unit 2 > Ackerman Lectures 9-10 > Flashcards

Flashcards in Ackerman Lectures 9-10 Deck (52):
1

fates for glucose

glycolysis, PPP, glycogenesis

2

sources of glucose

GNG, glycogenolysis

3

GNG tissues

liver (1o site-when liver glycogen is depleted, provides E to brain and RBCs); kidney cortex (supp glc to kidney medulla); skeletal muscle (used here b/c still G6P (not cleaved))

4

non-carb precursors

lactate (RBC glycolysis), AAs (Ala, not K or L), glycerol (from TAG), propionate (fr AAs or odd-chain FAs)

5

Cori cycle

relationship b/w liver GNG and RBC glycolysis; anaerobic feeder pathway (GNDG, glycolysis)

6

alanine cycle

relationship b/w liver GNG and skel musc glycolysis; aerobic feeder pathway (GNG, ureogenesis, glycolysis)

7

GNG vs glycolysis

must overcome irreversible steps (PK, PFK-1, HK/GK)

8

GNG sub for hexokinase/glucokinase

glucose-6-phosphatase; relevant to all non-carb glucose precursors; ONLY in liver; HK isozymes have diff affin for glucose

9

GNG sub for PFK-1

fructose 1,6-bisphosphatase; relevant to all non-carb glucose precursors; mult allosteric effectors, hormonal ctrl (insulin, glucagon)

10

GNG sub for pyruvate kinase

pyruvate carboxylase (mito matrix), req CO2, biotin, ATP; then PEP carboxykinase, GTP-dep kinase w/CO2 released; relevant to all rxns w/pyruvate AND TCA metabolites; liver PK under glucagon control

11

PEP carboxykinase

all glucogenic precursors except glycerol

12

pyruvate carboxylase

only glucogenic precursors that are metabolized to pyruvate

13

HK I

high affin for glucose; inhib by G6P, F6P (so inhib glycolysis)

14

HK IV (GK)

low affin for glucose; not inhib by G6P (liver glyc can occur simult w/high [G6P]

15

PFK-1 allosteric regulators

+ by ADP, AMP, F2,6BP; - by ATP, citrate (lipid synth-->amplifies ATP effect)

16

FBPase-1 allosteric regulators

- by AMP, F2,6BP

17

F26BP

ctrl'd by bifxnal enz; created by PFK-2; back to F6P by FBPase-2; cat at 2 sites in single polypep chain--homodimer

18

insulin effect on bifxnal enz

dephos-->activate PFK-2, inhib FBPase-2; C away from glucose (signal that glucose is high)

19

glucagon effect on bifxnal enz and PK

phos-->inhib PFK-2, stim FBPase-2 (signal that glucose is low, so C twd glucose); in liver PK, inactivates during GNG (ensures PEP used to make glucose, not pyr)

20

poly glucose advantages (alone and over TAG)

hexose monomers inc osmolarity, impede facil transport of new glc into cells; rapidly meets E needs, metab in pres/absence of O2, princ catab is glucose (fuel source for brain)

21

glycogen synthase

create a1-4 bonds (linear)

22

branching enzyme

create a1-6 bonds once a glucose a1-4 chain is at least 11 units long; inc solubility, inc number of nonred ends (facil further growth of polymer, expansion of E storage capacity)

23

glycogen phosphorylase

break a1-4 bonds (except those adj to branch points)

24

debranching transglycosylase

transfers a1-4 link from branch to main chain (makes accessible to glyc phosphorylase)

25

debranching glucosidase

breaks a1-6 bonds at branch points

26

UDP-glucose

activated intermediate of glycogenesis

27

glycogenin

primes glycogenesis pathway; self-glycosylating prot; remains at core of glycogen particle (so glycogen is proteoglycan)

28

glycogenesis

gluco/hexokinase; phosphoglucomutase; glucose 1-P uridylyltransferase; glycogen synthase; liver must be able to make G6P cont, even in high [G6P], to feed mult paths

29

glycogen synthase

cats elongation of glucose polymer; chem bond formation b/w C-1 glc monomer and C-4 of terminal gluc at non-red end of glycogen polymer

30

glycogenesis rxn

G1P + UTP --> UDP-glucose + PPi; UDP-glucose + (glucose)n --> UDP + (glucose)n+1; PPi-->2Pi

31

glycogenolysis

glycogen phosphorylase (leaves G1P), debranching enz (prod is glucose)

32

glycogen phosphorylase

cleaves non-red end of glycogen, releases phosphorylated glucose (G1P); cannot cleave a 4-glucose unit attached at an a1-6 branch point; end prod is glucose 1-P

33

transglycosylase/transferase of debranching enz

moves 3-glucose units to non-reducing end

34

acid a-glucosidase of debranching enz

cleaves a1-6 bond-->release glucose (hydrolysis, no phosphate involved), leaving unbranched a1-4 polymer for further phosphorylase axn

35

insulin reg of glycogen metabolism

activates of glycogenesis in liver and skel musc

36

glucagon reg of glycogen metabolism

activates of glycogenolysis in liver only

37

epinephrine reg of glycogen metabolism

activates glycogenolysis in liver and skel musc (via b-adren recep (cAMP/PKA) in both; by a-adren recep (PKC) in liver only)

38

nerve stimulation/contraction

signals glycogenolysis

39

stim glycogenolysis in liver

glucagon or epi (via a or b-adren recep) by activating phosphorylase kinase (PHOK)

40

stim glycogenolysis in skel musc

epi bds to b-adren recep; epi/b-adren recep/GPCR regulation mech; Ca activates PHOK, AMP activates GPHO; GPCR-->AC-->PKA-->PK-->GP

41

insulin-mediated regul of glycogenesis

phosphorylated glycogen synthase thru GSK3 is INACTIVE; PP1 activates GS; insulin inactivates GSK3, activates PP1 so GS active when insulin is around

42

high blood glucose

insulin-med events; store-glycogenesis active; activate glycolysis (E, route C from CHO to fat; DHAP precursor to glycerol backbone of TAG, citrate precursor to FAs of TAG)

43

low blood glucose

glucagone/epi-mediated events; message to liver-feed brain; message to musc-bring it on or get me out of here

44

type I GSD

glucose-6-phosphatase deficiency

45

type II GSD

acid a-glucosidase deficiency (debranching enz)

46

type III GSD

transglycosylase deficiency (debranching enz)

47

type IV GSD

branching enzyme deficiency

48

type V GSD

musc glycogen phosphorylase deficiency (m-GPHO)

49

type VI GSD

liver glycogen phosphorylase deficiency (l-GPHO)

50

type VII GSD

muscle phosphofructokinase deficiency (m-PFK1) deficiency

51

type IX GSD

phosphorylase kinase (PHOK) deficiency

52

type 0 GSD

glycogen synthase deficiency