Card Set Information
ch. 10 gluconeogenesis
Gluconeogenesis: synthesis of glucose from non carb sources
lactate, AA's that convert to pyruvate or TCA cycle intermed. and glycerol
at the end gluconeogenesis: 6 ATP are consumed
fructose, glactose, mannose, and ODD chain FA
realeased into blood by muscle and RBC
muscles convert glucose to lactate
Human glucose requirements?
and brain requirment?
: 75% of glucose in blood.
diag slide 3: liver/muscle- cori cycle
glucose from liver goes into muscle
muscle turns glucose into lactate
lactate goes into liver to turn into glucose
AA from tissue proteins
: most abundant AA
from hydrolysis of triacylglycerols in adipose tissue
from anaerobic glycolysis in muscle and erythrocytes
Location of gluconeo.
epithelium of intestine
In prolonged starvation
: kidneys have a bigger role
: mitochondria-pyruvate caboxylase rxn
: some parts
Function of gluconeo.
1. maintain blood glucose level in fasting state.
energy needs in brain, rbc, muscle, and renal medulla.
-reversal rxns of glycolysis excepts it's
-bypasses irreversible steps of glycolysis
the rxns catalyzed by
conversion of pyruvate to PEP
bypasses the irreversible pyruvate kinase rxn
pyruvate carboyxlase (step 1)
biotin containing mito. enzyme
converts pyruvate to oxaloacetate (OAA) an irreversible rxn that consumes ATP
: leads to buildup of pyruvate, and converted to lactic acid=lactic acidosis
is a reduced malate shuttle and transported to cytosol and reoxidized to OAA
step 2: PEP carboxykinase
decarboxylates OAA to PEP in rev. rxn that consumes GTP
***step 3: Fructose 1,6 bisphosphatase (rate limiting enzyme)
dephosphorylates F-1,6Bis to produce F-6-P which by passes irrev. PFK-1 rxn
low inulin/high glucagon: (fasting) leads to
high protein kinase effects bifunctional enzyme complex
low F-2-6-bis (FBP-2) levels (phospho form-active) and PFK-2 (phospho form-inactive) leads to decreased Fruc2,6bis phospahtase (FBP-1).
: low glycolysis in liver, high gluconeogenesis (maintains blood glucose)
FED state: high insulin/low glucagon leads to
low protein kinase
high f2,6Bis (FBP2- inactive) and (PFK2-active)
: high glycolysis in liver, low gluconeogenesis.
opposite effect on fruc1,6 bis and PFK-1
fructose 2,6 Bisph and AMP stimulate
pfk-1, increases glycolysis
fructose 2, 6 bis and AMP inhibit
F-1,6,bisphosphatase, decreases gluconeogenesis
detects either guconeogen. or glycolysis
positive allosteric effector or pyruvate carboxylase
diverts pyruvate into gluconeogenic path then to TCA
Allosterically activates hepatic pyruvate carboxylase , and leads to inc. gluconeogen.
stimulates conversion of pyruvate kinase to inactive form
affects pryvate formation from PEP
results in inc. of glucose synthesis.
gluconeogenic enzyme deficiency results in
provides 1/3 of C to gluconeo.
lactate from muscle and RBC travels to liver to turn to glucose, then travels back to muscle and RBC.
glucogenic AA derived from
degradation of muscle proteins (protein metabolism)
important source for of C for gluconeogen in fasting.
glycerol kinase in liver converts
is used as a substrate for gluconeogen.
10.1 synthesis of glucose from pyruvate by gluconeogen requires
10.2 True statement for gluconeogenesis
important in maintaining blood glucose during normal overnight fast.
10.3 unique rxn
oxalocetate --> phosphoenolpyruvate
10.4 metabolism of ethanol by alcohol dehydrogenase (ADH) produce NADH. what effect of change in NAD/NADH has on gluconeogen
2 substrates (OAA and pyruvate) are decreased as a result of inc. NADH
therefore, gloconeo. decreases.
10.5 acetyl CoA cannot be substrate for gluconeo, why is production of fatt acid oxidation essential for gluconeo.
Acetyl CoA inhibits pyruvate dehyd and activates pyruvate cabox.
pushes pyruvate to gluconeogen.
10.6 what does AMP do for gluconeo. and glycolysis? what enzymes are effected?
AMP inhibs gluconeo by inhibiting fr-1,6bis
favors glycolysis through activation of phosphofructokinase-1
f2,6bis has same effect