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Glycogen Metabolism

Glycogen Metabolism. Glycogenesis. What? G6P + (glycogen) n  (glycogen) n+1 Why? Store glucose as a fuel reserve Where? Liver and muscle cells When? Fed state (insulin present and blood glucose level high). Glycogenolysis. What? (glycogen) n+1  G6P + (glycogen) n Why? Where? When? .

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Glycogen Metabolism

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  1. Glycogen Metabolism

  2. Glycogenesis • What? G6P + (glycogen)n (glycogen)n+1 • Why? Store glucose as a fuel reserve • Where? Liver and muscle cells • When? Fed state (insulin present and blood glucose level high)

  3. Glycogenolysis • What? (glycogen)n+1 G6P + (glycogen)n • Why? • Where? • When?

  4. Electron micrograph of a liver cell

  5. Glycogen metabolism overview

  6. Enzymes needed for glycogen breakdown

  7. Enzymes needed for glycogen breakdown

  8. Enzymes needed for glycogen breakdown • Phosphoglucomutase: converts G1PG6P

  9. Muscle phosphorylase

  10. Liver phosphorylase

  11. Phosphorylase kinase: phosphorylates phosphorylase

  12. Glycogen synthesis and degradation have different pathways • Flexibility in energetics control • Synthesis: Glycogenn + UDP-glucoseglycogenn+1 + UDP • Degradation: Glycogenn+1 + Pi  glycogenn + glucose-1-P

  13. Glycogen synthase

  14. Branching enzyme forms a-1,6 links

  15. Glycogen breakdown and synthesis are reciprocally regulated

  16. Glycogen metabolism in the liver regulates blood glucose level

  17. PPP generates NADPH

  18. Oxidative phase of PPP

  19. PPP and Glycolysis are linked by transketolase and transaldolase 5 5 3 7

  20. PPP and Glycolysis are linked by transketolase and transaldolase 3 7 6 4

  21. PPP and Glycolysis are linked by transketolase and transaldolase 4 5 6 3

  22. FA synthesis • What? 8 acetyl CoA + 14 NADPH + 7 ATP  palmitate + 8 CoASH • Why? Synthesize FA for energy storage as TAGs in adipose • Where? Adipose and liver • When? Fed state (insulin present, blood glucose level high)

  23. Adipocyte TAGs

  24. FA synthesis: committed step • Acetyl CoA + ATP + HCO3- malonylCoA + ADP + Pi + H+

  25. FA synthesis

  26. FA synthesis

  27. FA synthesis

  28. FA synthesis: end 1st round

  29. b Oxidation • Palmitate + 8 CoASH + 7 NAD+ + 7 FAD + ATP  8 Acetyl CoA + 7 NADH + 7 FADH2 + AMP • Why? Allows ATP to be made from FADH2, NADH and acetyl CoA • Where? Most cells (excluding brain) • When? Fasting state (glucagon stimulates lipase activity in adipose)

  30. Lipolysis occurs in adipose tissue

  31. Lipolysis

  32. Glycerol from lipolysis is absorbed by the liver

  33. Glycerol from lipolysis is absorbed by the liver

  34. Glycerol from lipolysis is absorbed by the liver and converted to GAP

  35. FA linked to CoA before oxidation Rxn occurs on outer mito membrane

  36. FA must enter matrix to be oxidized

  37. FA (b) oxidation • Each Round: • Shorten by 2-C • Acetyl CoA • NADH • FADH2

  38. Dehydrogenase

  39. Hydratase

  40. Dehydrogenase

  41. b-ketothiolase

  42. 3 rounds of palmitate degradation

  43. Oxidation of palmitoyl CoA • Palmitoyl CoA + 7 FAD + 7 NAD+ + 7 CoA + 7 H2O  8 acetyl CoA + 7 FADH2 + 7 NADH + 7 H+ • 7 FADH2 = 10.5 ATP • 7 NADH = 17.5 ATP • 8 acetyl CoA = 80 ATP • 2 ATP used in palmitate activation • 106 ATP from complete oxidation of palmitate

  44. Ketone body formation • 2 acetyl CoA KBs (acetoacetate, acetone & b-hydroxybutyrate) • Why? KBs can be exported to blood and used as fuel instead of glucose • Where? Liver • When? Late/long-term fasting state (simultaneous with gluconeogenesis)

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