Abstract

The mechanisms by which actinomycin D and cycloheximide administration prevents the accumulation of glycogen caused by testosterone in the rat levator ani muscle (LAM) have been investigated. Actinomycin D administration only slightly inhibits the effects of testosterone on the xylose uptake and the sugar phosphorylation by the LAM, but it markedly inhibits the increase of the rate of glycogen synthesis by blocking the effect of the hormone on the conversion of glycogensynthetase to the I (physiologically active) form. Evidences have been found indicating that actinomycin D effect might be due to its specific action on RNA synthesis; therefore, even though the interpretation of the effects of inhibitors administered in vivo must be cautious, it is possible to suggest that a normal RNA synthesis is needed to allow testosterone effect on glycogen synthetase to appear. This does not necessarily imply that testosterone acts by inducing enzyme synthesis. Cycloheximide administration leads to a marked inhibitio...

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