Insulin-stimulated glycogen synthesis and glycogen synthase activation after electrical stimulation of epitrochlearis muscles with different initial glycogen contents

Abstract

Glycogen synthesis increases after muscle contraction and during insulin stimulation, and insulin-stimulated glycogen synthesis is enhanced after contraction. We hypothesized that the initial glycogen content influences the magnitude of additive effect of contraction on insulin-stimulated glycogen synthesis. Contraction and insulin had full additive effect on rate of glycogen synthesis measured after contraction in muscles with normal and high glycogen content. In muscles with low glycogen, contraction increased insulin-stimulated glycogen synthesis nearly as much as in muscles with normal glycogen, but not to the sum of the two stimuli studied separately; still glycogen synthesis was generally highest in muscles with low glycogen. Glycogen synthase fractional activity inversely correlated with glycogen content and contraction increased glycogen synthase fractional activity. Contraction and insulin additively increased glycogen synthase fractional activity at all glycogen contents. In conclusion, after contraction insulin-stimulated glycogen synthesis was increased by rather similar magnitude at all glycogen contents in concert with increased glycogen synthase activation.

Keywords::

• PKB
• p38MAP-kinase
• GSK-3
• phosphorylation
• enzyme kinetic
• UDP-glucose
• affinity

Acknowledgements

We thank Ada Ingvaldsen and Astrid Bolling for technical assistance in some of the experiments. The study supported by Novo Nordisk Foundation. J.J. is supported via participation in the EU funded COST Action BM0602.