CH 10

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smartguy
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224259
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CH 10
Updated:
2013-06-18 10:14:27
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gluconeogenesis
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ch. 10 gluconeogenesis
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  1. Gluconeogenesis: synthesis of glucose from non carb sources
    Precursors:
    lactate, AA's that convert to pyruvate or TCA cycle intermed. and glycerol

    at the end gluconeogenesis: 6 ATP are consumed
  2. Fuels:
    fructose, glactose, mannose, and ODD chain FA
  3. Lactate
    realeased into blood by muscle and RBC
  4. Cori cycle
    muscles convert glucose to lactate
  5. Human glucose requirements?
    and brain requirment?
    • per day: 1mole=180g
    • brain: 75% of glucose in blood.
  6. 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
  7. gluconeo substrates
    • AA from tissue proteins
    • Glycerol
    • lactate
  8. AA's
    • alanine: most abundant AA
    • glutamine
    • asparatate
  9. Glycerol
    from hydrolysis of triacylglycerols in adipose tissue
  10. lactate
    from anaerobic glycolysis in muscle and erythrocytes
  11. 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
  12. Function of gluconeo.
    • 1. maintain blood glucose level in fasting state.
    • energy needs in brain, rbc, muscle, and renal medulla.
  13. Pathway
    • -reversal rxns of glycolysis excepts it's
    • irreversible steps

    -bypasses irreversible steps of glycolysis

    • the rxns catalyzed by:
    • -hexokinase
    • -phosphofructokinase
    • -pyruvate kinase
  14. conversion of pyruvate to PEP
    bypasses the irreversible pyruvate kinase rxn
  15. 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
  16. oxaloacetate (OAA)
    is a reduced malate shuttle and transported to cytosol and reoxidized to OAA
  17. step 2: PEP carboxykinase
    decarboxylates OAA to PEP in rev. rxn that consumes GTP
  18. ***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
  19. slide 14: 
    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)
  20. 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.
  21. Allosteric effects
    opposite effect on fruc1,6 bis and PFK-1
  22. fructose 2,6 Bisph and AMP stimulate
    pfk-1, increases glycolysis
  23. fructose 2, 6 bis and AMP inhibit
    F-1,6,bisphosphatase, decreases gluconeogenesis
  24. reciprocal regulation
    detects either guconeogen. or glycolysis
  25. Acetyl CoA
    • positive allosteric effector or pyruvate carboxylase
    • diverts pyruvate into gluconeogenic path then to TCA
    • Allosterically activates hepatic pyruvate carboxylase , and leads to inc. gluconeogen.
  26. Glucagon
    • stimulates conversion of pyruvate kinase to inactive form
    • affects pryvate formation from PEP
    • results in inc. of glucose synthesis.
  27. gluconeogenic enzyme deficiency results in
    fasting hypglycemia
  28. lactate
    provides 1/3 of C to gluconeo.
  29. Cori cycle
    lactate from muscle and RBC travels to liver to turn to glucose, then travels back to muscle and RBC.
  30. glucogenic AA derived from
    degradation of muscle proteins (protein metabolism)
  31. Glycerol
    important source for of C for gluconeogen in fasting.
  32. glycerol kinase in liver converts
    • glycerol to DHAP
    • DHAP is used as a substrate for gluconeogen.
  33. 10.1 synthesis of glucose from pyruvate by gluconeogen requires
    Biotin
  34. 10.2 True statement for gluconeogenesis
    important in maintaining blood glucose during normal overnight fast.
  35. 10.3 unique rxn
    oxalocetate --> phosphoenolpyruvate
  36. 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.
  37. 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.
  38. 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

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