Ackerman Lectures 9-10 Flashcards
fates for glucose
glycolysis, PPP, glycogenesis
sources of glucose
GNG, glycogenolysis
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))
non-carb precursors
lactate (RBC glycolysis), AAs (Ala, not K or L), glycerol (from TAG), propionate (fr AAs or odd-chain FAs)
Cori cycle
relationship b/w liver GNG and RBC glycolysis; anaerobic feeder pathway (GNDG, glycolysis)
alanine cycle
relationship b/w liver GNG and skel musc glycolysis; aerobic feeder pathway (GNG, ureogenesis, glycolysis)
GNG vs glycolysis
must overcome irreversible steps (PK, PFK-1, HK/GK)
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
GNG sub for PFK-1
fructose 1,6-bisphosphatase; relevant to all non-carb glucose precursors; mult allosteric effectors, hormonal ctrl (insulin, glucagon)
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
PEP carboxykinase
all glucogenic precursors except glycerol
pyruvate carboxylase
only glucogenic precursors that are metabolized to pyruvate
HK I
high affin for glucose; inhib by G6P, F6P (so inhib glycolysis)
HK IV (GK)
low affin for glucose; not inhib by G6P (liver glyc can occur simult w/high [G6P]
PFK-1 allosteric regulators
+ by ADP, AMP, F2,6BP; - by ATP, citrate (lipid synth–>amplifies ATP effect)
FBPase-1 allosteric regulators
- by AMP, F2,6BP
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
insulin effect on bifxnal enz
dephos–>activate PFK-2, inhib FBPase-2; C away from glucose (signal that glucose is high)
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)
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)