Insulin-independent glycogen supercompensation in isolated mouse skeletal muscle: role of phosphorylase inactivation.
Glycogen supercompensation (increase in muscle glycogen content above basal) is an established phenomenon induced by unknown mechanisms. It consists of both insulin-dependent and -independent components. Here, we investigate insulin-independent glycogen supercompensation in isolated, intact extensor digitorum longus muscles from mice. Muscles were stimulated electrically, incubated in vitro with 5.5 mM glucose for up to 16 h and then analysed for glycogen, glucose uptake and enzyme activities. Basal glycogen was 84+/-6 micro mol glucosyl units/g dry muscle and was depleted by 80% after 10 min contraction. Glycogen increased after contraction, reaching a peak value of 113+/-9 micro mol glucosyl units/g dry muscle ( P<0.05 vs. basal) by 6 h, and returned to basal values by 16 h (84+/-8). Maximal activities of glycogen synthase, phosphorylase and alpha-glucosidase were not significantly altered by contraction or during the 6-h recovery period. Glycogen synthase fractional activity (0.17/7.2 mM glucose-6-P; inversely related to phosphorylation state of the enzyme) was increased about twofold early after contraction but then decreased and was slightly lower than baseline during the period of supercompensation (4-6 h). Phosphorylase fractional activity (+/-adenosine monophosphate; directly related to phosphorylation state of the enzyme) decreased to 60% of basal after contraction and decreased further during the initial 4 h of recovery to 40% of basal ( P<0.01 vs. basal). After 4 h recovery, glucose uptake was slightly (50%) higher in the stimulated than in the non-stimulated muscle ( P<0.01). Thus, insulin-independent glycogen supercompensation involves inactivation of phosphorylase and hence an inhibition of glycogen breakdown.
Sandström
Marie E
ME
Department of Physiology and Pharmacology, Karolinska Institutet, Von Eulers väg 8, 17177 Stockholm, Sweden.
Abbate
Fabio
F
Andersson
Daniel C
DC
Zhang
Shi-Jin
SJ
Westerblad
Håkan
H
Katz
Abram
A
D000818:Animals; D002478:Cells, Cultured; D004558:Electric Stimulation; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000032:analysis / Q000378:metabolism*; D024982:Glycogen Phosphorylase, Muscle Form / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D008297:Male; D051379:Mice; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000737:chemistry / Q000502:physiology*; D000520:alpha-Glucosidases / Q000378:metabolism
D007328:Insulin; D006003:Glycogen; D024982:Glycogen Phosphorylase, Muscle Form; D000520:alpha-Glucosidases; D005947:Glucose