The breakdown of glycogen in the lysosomes of newborn rat hepatocytes: the effects of glucose, cyclic 3',5'-AMP and caffeine.

The effects of parenteral glucose, cyclic AMP and caffeine on the breakdown of glycogen in the lysosomes of newborn rat hepatocytes, were studied by using biochemical assays, electron microscopy and quantitative morphometry. Glucose prevented the normal postnatal increase in lysosomal volume, acid alpha 1,4 glucosidase activity and lysosomal glycogen breakdown. On the contrary, cyclic AMP and caffeine promoted this increase. There was a positive correlation between liver cyclic AMP concentration and acid glucosidase activity (R = 0.84, p < 0,001). Cyclic AMP also induced a change in the shape of lysosomes. The postulation that glucagon secreted after birth is the natural stimulus for the cyclic AMP-mediated postnatal increase in acid glucosidase activity and mobilization of the lysosomal glycogen in rat hepatocytes, is supported by these experimental findings.

A quantitative description of the insulin-induced ultrastructural changes in newborn rat hepatocytes.

The effects of insulin on the ultrastructure of newborn rat hepatocytes were systematically quantified at satisfactory statistical significance. Insulin prevented the normal postnatal increase in the total volume of lysosomes and the breakdown of glycogen inside these organelles. The lysosomal glycogen-hydrolysing enzyme, acid alpha 1,4 glucosidase was inhibited by the hormone. Insulin also prevented the normal postnatal increase in the total volume of peroxisomes, especially of the crystalloid core-devoid type. The hormone produced an increase in the area of cell membrane, due to the formation of many irregular folds of the cell surface. These results constitute good evidence for participation of lysosomes and peroxisomes in the overall glycogen degradation and or gluconeogenesis in the newborn rat hepatocytes.