Ackerman Lectures 9-10 Flashcards

(52 cards)

1
Q

fates for glucose

A

glycolysis, PPP, glycogenesis

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2
Q

sources of glucose

A

GNG, glycogenolysis

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3
Q

GNG tissues

A

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))

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4
Q

non-carb precursors

A

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

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5
Q

Cori cycle

A

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

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6
Q

alanine cycle

A

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

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7
Q

GNG vs glycolysis

A

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

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8
Q

GNG sub for hexokinase/glucokinase

A

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

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9
Q

GNG sub for PFK-1

A

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

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10
Q

GNG sub for pyruvate kinase

A

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

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11
Q

PEP carboxykinase

A

all glucogenic precursors except glycerol

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12
Q

pyruvate carboxylase

A

only glucogenic precursors that are metabolized to pyruvate

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13
Q

HK I

A

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

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14
Q

HK IV (GK)

A

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

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15
Q

PFK-1 allosteric regulators

A

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

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16
Q

FBPase-1 allosteric regulators

A
  • by AMP, F2,6BP
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17
Q

F26BP

A

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

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18
Q

insulin effect on bifxnal enz

A

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

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19
Q

glucagon effect on bifxnal enz and PK

A

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)

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20
Q

poly glucose advantages (alone and over TAG)

A

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)

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21
Q

glycogen synthase

A

create a1-4 bonds (linear)

22
Q

branching enzyme

A

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
Q

glycogen phosphorylase

A

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

24
Q

debranching transglycosylase

A

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