glycogen. human liver - 50 g/kg wet wt. skeletal muscle - 15 g/kg wet wt. glycogenin = protein core...
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Glycogen
Human liver - 50 g/kg wet wt.
Skeletal muscle - 15 g/kg wet wt.
Glycogenin = protein core
Glycosome
~
~
1-4 bonds1-6 bonds
Glycoside bonds
Proglycogen (acid insoluble)
Macroglycogen (acid soluble)
Size = glycogenin – Proglycogen – Macroglycogen
12 tiers is the maximum – branches too dense to allow GS
Tier 8
Lomako, et al., FASAB J. 9, 1126-1137, 1995
Macroglycogen
Proglycogen
Glygogenin
Two Forms of Muscle Glycogen
75% proglycogen/25% macroglycogen
Glycogen SynthesisGlycogen Synthase 1-4 bonds
Glycosyl 4:6 transferase
Branching enzyme(at least 11)
( leave at least 4)(move at least 7)
1-4 Bond1-6 Bond
Glycogenolysis
(Glucose-1-P Glucose-6-P)(phosphoglucomutase)
phosphorylaseGlucose -6-P
to glycolysis
glycosyl 4:4 transferase(breaks a 1-4, makes a 1-4)
(NEXT)
a b c
fed
a b c
a b c fed
Glycogenolysis (cont.)
a b cto another chain
free glucose
Amylo 1:6 glucosidase
a b c
fed
glycosyl 4:4 transferase
a b c
free 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
Glycogenolysis- the break down of glycogen into glucose
Summary
Summary• 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
Three CHO-Loading Protocols:Two Depletion & One Taper
Saltin and Hermansen, Nut. Physical Activity, pp.32-46, 1967
Phosphorylates glycogen synthase
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.
Active Inactive
- P
Insulin activates PP-1 and PDE (phosphodiesterase). This will decrease C-AMP and dephosphorylate proteins that were phosphorylated by PKA
Lomako, et. al.,FASAB 7:1386-1393
Order of Glycogen Resynthesis
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.
Casey, et al., J.Physiol. 48(1): 265-271, 1995.
Rapid Phase – increased insulin sensitivity GLUT 4 from exercise
Slow Phase- dependent on insulin concentration
EFFECT of DETRAINING on MUSCLE GLYCOGEN CONCENTRATIONS
Costill, et., al., Med. Sci. Sports Exerc., 17(3):339-343, 1985.
60%80% 72%100%
Costill, et. al., J.A.P. 31(6): 834-838, 1971.
Muscle Glycogen During 3 days of Endurance Training and al Low-CHO vs High-CHO Diet