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Departments of 1 Internal Medicine and 2 Diagnostic Radiology and the 3 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510
To examine the mechanism by which muscle
glycogen limits its own synthesis, muscle glycogen and glucose
6-phosphate (G-6-P) concentrations were measured in seven
healthy volunteers during a euglycemic (~5.5 mM)-hyperinsulinemic
(~450 pM) clamp using 13C/31P nuclear
magnetic resonance spectroscopy before and after a muscle glycogen
loading protocol. Rates of glycogen synthase
(Vsyn) and phosphorylase
(Vphos) flux were estimated during a
[1-13C]glucose (pulse)-unlabeled glucose (chase)
infusion. The muscle glycogen loading protocol resulted in a 65%
increase in muscle glycogen content that was associated with a twofold
increase in fasting plasma lactate concentrations (P < 0.05
vs. basal) and an ~30% decrease in plasma free fatty acid
concentrations (P < 0.001 vs. basal). Muscle glycogen
loading resulted in an ~30% decrease in the insulin-stimulated rate
of net muscle glycogen synthesis (P < 0.05 vs. basal),
which was associated with a twofold increase in intramuscular
G-6-P concentration (P < 0.05 vs. basal). Muscle
glycogen loading also resulted in an ~30% increase in whole body
glucose oxidation rates (P < 0.05 vs. basal), whereas there was no effect on insulin-stimulated rates of whole body glucose uptake
(~10.5 mg · kg body
wt
1 · min1 for both clamps)
or glycogen turnover
(Vsyn/Vphos was ~23% for both clamps). In conclusion, these data are consistent with the hypothesis that glycogen limits its own synthesis through feedback inhibition of glycogen synthase activity, as reflected by an
accumulation of intramuscular G-6-P, which is then shunted into
aerobic and anaerobic glycolysis.
nuclear magnetic resonance spectroscopy; glycogen turnover; glycogen synthase
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