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Glycogen

Glycogen. ~. Human liver - 50 g/kg wet wt. ~. Skeletal muscle - 15 g/kg wet wt. Glycogenin = protein core Glycosome.  1-4 bonds 1-6 bonds Glycoside bonds. Tier 8. Proglycogen (acid insoluble) Macroglycogen (acid soluble). Size = glycogenin – Proglycogen – Macroglycogen

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Glycogen

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  1. Glycogen

  2. ~ Human liver - 50 g/kg wet wt. ~ Skeletal muscle - 15 g/kg wet wt. Glycogenin = protein core Glycosome

  3.  1-4 bonds • 1-6 bonds Glycoside bonds

  4. Tier 8 Proglycogen (acid insoluble) Macroglycogen (acid soluble) Size = glycogenin – Proglycogen – Macroglycogen 12 tiers is the maximum – branches too dense to allow GS

  5. Two Forms of Muscle Glycogen Proglycogen Macroglycogen Glygogenin Lomako, et al., FASAB J. 9, 1126-1137, 1995 75% proglycogen/25% macroglycogen

  6. Glycogen SynthesisGlycogen Synthase 1-4 bonds Glycosyl 4:6 transferase Branching enzyme (at least 11) (move at least 7) ( leave at least 4)

  7. Glycogenolysis 1-6 Bond 1-4 Bond (Glucose-1-P Glucose-6-P) (phosphoglucomutase) phosphorylase Glucose -6-P a b c d e f a b c glycosyl 4:4 transferase (breaks a 1-4, makes a 1-4) to glycolysis (NEXT)

  8. Glycogenolysis (cont.) a b c d e f a b c glycosyl 4:4 transferase a b c d e f to another chain a b c Amylo 1:6 glucosidase free glucose free glucose

  9. Summary Glycogenolysis- the break down of glycogen into glucose Glycogen Synthesis- the storage of glucose via glycogen formation -Glycogen Synthase- enzyme responsible for making  1-4 bonds between glucose molecules -Glycosyl 4:6 transferase- enzyme that breaks  1-4 bonds, and makes  1-6 bonds to allow for branching

  10. Skeletal Muscle Epi/N-Epi (beta receptor)  C-AMP  Ca++ (actives phosphorylase kinase These will increase activity of phosphorylase and decrease glycogen synthase Insulin  PDE activity which will decrease C-AMP  PP-1 which will increase the activity of GS and decrease the activity of phosphorylase Summary

  11. Three CHO-Loading Protocols: Two Depletion & One Taper Saltin and Hermansen, Nut. Physical Activity, pp.32-46, 1967

  12. Phosphorylates glycogen synthase

  13. CA++ actives Phosphorylase Kinase at the start of exercise by 20x. Ca++ binds to gamma subunit of PK. Phosphorylase Kinase activated via C-AMP and PKA. Phosphorylase kinase phosphorylates Phosphorylase at serine 14. AMP allosterically actives Phosphorylase.

  14. Inactive Active - P Insulin activates PP-1 and PDE (phosphodiesterase). This will decrease C-AMP and dephosphorylate proteins that were phosphorylated by PKA

  15. Order of Glycogen Resynthesis Lomako, et. al.,FASAB 7:1386-1393

  16. Glycogen Storage Diseases Type I: Von Gierke Disease; Glucose-6-phosphatase Defect • Hypoglycemia occurs due to defect of the final step of gluconeogenesis. • This disease, affects only liver and renal tubule cells • Decreased mobilization of glycogen produces hepatomegaly. Type V: McArdle Disease; Skeletal Muscle Glycogen Phosphorylase Defect • Skeletal muscle is affected, whereas the liver enzyme is normal. • Exercise capacity is greatly reduced, hypoglycemia during exercise • There is no rise in blood lactate during strenuous exercise. • Muscle contains a high level of glycogen with normal structure • Type VI: Hers Disease; Liver Glycogen Phosphorylase Defect • Liver is affected, whereas the skeletal muscle enzyme is normal. • Marked hepatomegaly occurs due to a high level of glycogen with normal structure.. • Following administration of glucagon, there is no increase in blood glucose.

  17. Slow Phase- dependent on insulin concentration Rapid Phase – increased insulin sensitivity GLUT 4 from exercise Casey, et al., J.Physiol. 48(1): 265-271, 1995.

  18. EFFECT of DETRAINING on MUSCLE GLYCOGEN CONCENTRATIONS 100% 80% 72% 60% Costill, et., al., Med. Sci. Sports Exerc., 17(3):339-343, 1985.

  19. Muscle Glycogen During 3 days of Endurance Training and al Low-CHO vs High-CHO Diet Costill, et. al., J.A.P. 31(6): 834-838, 1971.

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