Hepatic glycogen metabolism in normal developing and intrauterine growth-retarded rat fetuses.

The control of hepatic glycogen metabolism and storage was studied in normal developing and intrauterine growth-retarded (IUGR) rat fetuses during the last period of gestation with reference to the amount of total and active forms of synthase and phosphorylase enzymes. Glycogen in the hepatocytes was also studied at light and electron microscopic levels using special histochemical stainings. Body weight, liver weight, and liver glycogen increased progressively in both normal and IUGR fetuses. However, the increase rates were significantly lower in IUGR fetuses than in the normal group on days 20 and 21 of gestation (p less than 0.01). The activity of total and active forms of glycogen synthase and phosphorylase enzymes increased with the gestational days in both groups, and were significantly lower in the IUGR group than in the normal group on days 18 to 21 of gestation (p less than 0.001). The active synthase (I/I + D) and active phosphorylase (a/a + b) enzyme percentage was lower in IUGR group (6.9% and 32.1%) than in the normal group (7.83% and 36.7%) on day 21 of gestation. Analysis of the hepatocytes for glycogen by light and electron microscopy further supported the biochemical findings. It was suggested that the lower hepatic glycogen storage in the IUGR group may be due to the decreased activity of synthase enzymes, particularly the active form (I). Furthermore, the development of neonatal hypoglycemia in the IUGR fetuses may be attributed to the inadequate glycogen deposits and decreased activity of phosphorylase enzymes, especially the active form (a) in liver.