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36 Cards in this Set
- Front
- Back
3 important molecules that are crossroads in lipid/carb metabolism:
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-Glucose 6 phosphate
-AcCoA -Pyruvate |
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5 main enzymes under allosteric control:
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Glycolysis: PFK1, FBPase
FA Biosnth: AcCoA Carboxylase Pyruvate: PDH Pyruvate: Pyruvate Carboxylase |
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Allosteric effectors of PFK1:
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Negative: Citrate (sends G6P to gluconeogenesis instead)
Negative: ATP Positive: F26BP |
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Allosteric effectors of FBPase1:
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Negative: F26BP
Positive: ATP |
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Result of active PFK1:
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Glycolysis
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Result of active FBPase1:
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Gluconeogenesis
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Allosteric effectors of AcCoA Carboxylase:
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Positive: Citrate
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Allosteric effector PRODUCED BY AcCoA Carboxylase:
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Malonyl CoA
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Effect of Malonyl CoA
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Inhibits CPT1 - turns off FA b-oxidation
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Allosteric effectors of PDH:
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-Neg Feedback of NADH, AcCoA
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NADH inhibits:
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-PDH
-TCA Isocitrate dehydrogenase -TCA Aketoglutarate dehydrogense |
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Allosteric effectors of Pyruvate Carboxylase
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AcCoA Activates it
(as PDH is turned off AcCoA shuttles into gluconeogenesis) |
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What allows Covalent regulation?
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Glucagon:insulin ratio
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Glucagon phosphorylation will ACTIVATE 3 things:
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-Glycogen phosphorylase (use glycogen stores)
-FBPase2 (turn off glycolysis) -Hormone sensitive Lipase (HSL) (turn on |
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Glucagon phosphorylation will INACTIVATE 3 things:
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-Glycogen synthase
-PFK2 -Pyruvate kinase |
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AMPK
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special phosphorylator for AcCoA Carboxylase
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What activates AMPK
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AMP
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What is the effect of AMPK:
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Phosphorylation = inactive AcCoA Carboxylase -> no FA biosynth
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Molecule that counteracts the effect of AMPK to some degree:
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Citrate - if it's building up from TCA, will shuttle to cytosol and allow FA biosynth in spite of high AMP levels.
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Covalent regulation of PDH
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-Personal phosphorylator
-Inactivates E1 |
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What activates the phosphorylator of PDH?
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-AcCoA
-NADH -ATP |
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So the effect of High energy on Pyruvate pools:
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1. Kinase phosphorylates PDH (-)
2. Pyruvate not used by TCA 3. Shuttle to gluconeogenesis |
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Effect of LOW energy on pyruvate pools:
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1. Kinase inactive; PDH +
2. TCA works |
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Long term Regulation of gluconeogenesis:
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PEPCK gene
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How is PEPCK gene regulated?
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-Responds to binding elements (Ins/Cort/Epi/cAMP)
-Changes concentration of enzyme |
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What allows for coordinated regulation of many pathway enzymes at once?
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SRE - serum response element
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4 enzymes controlled by SRE for FA biosynthesis:
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1. ATP-Citrate Lyase
2. Malic enzyme 3. AcCoA Carboxylase 4. FAS (FA Synthase) |
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2 reactions of TCA shut off by NADH:
(what else turns them off?) |
1. Isocitrate Dehydrog
2. a-Ketoglutarate Dehydrog (Incr ATP/ADP turns off too) |
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3 Pathways in Cytosol:
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1. Glycolysis
2. FA Biosynth 3. PPP |
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4 Pathways in Mitochondria
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1. FA oxidation
2. TCA 3. Oxidative phosphorylation 4. Ketone formation |
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2 Pathways that interplay between mito and cyto:
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1. Gluconeogenesis
2. Urea synthesis |
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How AcCoA pool converts from TCA to gluconeogenesis:
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AcCoA activates Pyruvate Carboxylase
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What does Pyruvate Carboxylase do?
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AcCoA -> Oxaloacetate that gets sent to cytosol for gluconeogenesis or ketogenesis.
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What molecule is specific for adipocytes and involved in Fat mobilization?
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HSL - hormone sensitive lipase
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What activates HSL?
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Glucagon/cAMP/PKA phosphorylation
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What is the effect of insulin on HSL?
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Inactive - if you're fed you don't need to be using your fat stores.
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