• 1 January 1976
    • journal article
    • research article
    • Vol. 199  (3) , 565-574
Abstract
The effects of uridine and inosine on glucose metabolism in rat diaphragm muscle incubated in Krebs-bicarbonate buffer were studied. Uridine in concentrations of 10-4-10-6 M stimulated the uptake of glucose and increased the content of glycogen, but had no effect on the production of lactate. When diaphragm muscles were incubated in the buffer without glucose, uridine (10-4-10-6 M) had no effects on the content of glycogen and on the production of lactate. Inosine in concentrations of 10-4-10-6 M stimulated the uptake of glucose and the production of lactate, but had no effect on the content of glycogen in the muscle. In a 2nd series of experiments, uridine (10-4-10-5 M) and inosine (10-4-10-7 M) inhibited the release of glycerol from isolated rat epididymal adipose tissue in Krebs-bicarbonate buffer. Uridine and inosine in concentrations of 10-4 M inhibited the epinephrine (10-5 M)-, the norepinephrine (10-5 M)- and the theophylline (10-3 M)-stimulated lipolysis. Dibutyryl cyclic AMP-stimulated lipolysis was further activated in the presence of 10-4 M uridine or inosine. Dose-response curves studies suggested that inosine, but not uridine, has a common receptor site with epinephrine in adipose tissue. Both nucleosides stimulated the glucose uptake, but only uridine increased the synthesis of glycogen in the muscle. Both nucleosides also inhibited lipolysis in adipose tissue. The mechanism of antilipolytic action of these nucleosides is unknown, but 1 of the receptor sites for inosine might be adenylate cyclase.