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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?
- per day: 1mole=180g
- brain: 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
- alanine: most abundant AA
from hydrolysis of triacylglycerols in adipose tissue
from anaerobic glycolysis in muscle and erythrocytes
Location of gluconeo.
- Liver 90%
- kidneys 10%
- epithelium of intestine
- In prolonged starvation: kidneys have a bigger role
- Occurs in: mitochondria-pyruvate caboxylase rxn
- cytosol: 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
- irreversible steps
-bypasses irreversible steps of glycolysis
- the rxns catalyzed by:
- -pyruvate kinase
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
- Biotin deficiency: 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).
- result: 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)
- Result: 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
- glycerol to DHAP
- DHAP 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