Abstract
1. The glycogen formed in the livers of adult rats was labelled by injection of [1-14C] galactose soon after initiation of re-feeding after starvation. The rats were anaesthetized 4h later and glycogenolysis was induced by giving them a mixture of glucagon and insulin. In confirmation of previous work [Devos & Hers (1979) Eur J. Biochem. 99, 161-167],, there was a delay in degradation of the labelled glycogen by comparison with total glycogen. This pattern is considered as characteristic of an ordered glycogenolysis. Treatment of rats with phlorizin abolished the difference between the fate of labelled and total glycogen, causing, therefore, a random glycogenolysis. 2. Foetal liver glycogen was made radioactive by injecting [14C] glucose into the mother at the 19.5 day of gestation, i.e. at the time when this glycogen starts to be synthesized. During the postnatal degradation of this glycogen, radioactive and total glycogen were degraded at approximately the same rate, indicating that glycogenolysis occurred at random. In contrast, when puromycin was injected into the newborn rats, there was a delay in he degradation of the labelled glycogen as compared with that of total glycogen, as currently observed in the normal adult liver. 3. These data are discussed in relation with the fact that glycogen-filled vacuoles are currently seen in the livers of adult rats treated with phlorizin, and also in the neonatal livers, and that puromycin is known to cause the disappearance of these autophagic pictures in the liver of newborn rats. It is suggested that random glycogenolysis occurs through hydrolysis by the lysosomal acid alpha-glucosidase, in the course of autophagy.