THE SEQUENTIAL RESTORATION OF PLASMA METABOLITE LEVELS, LIVER COMPOSITION AND LIVER STRUCTURE IN REFED CARP, CYPRINUS-CARPIO

Effect of realimentation was studied on the structure and function of liver tissue of carp, Cyprinus carpio. Yearling carp, after a 3-month starvation period, were renourished at a feeding rate of 1% body weight per day. Samples were taken at refeeding days 0, 1, 2, 5, 22 and 78. Analyses were made of blood metabolites, liver RNA, DNA, lipids, glycogen and protein and of liver enzyme activities. Additionally, liver cytology was examined by means of qualitative and quantitative electron microscopy. The early refeeding period (up to day 5) was characterized by a fast recovery of plasma metabolite concentrations (protein, total lipids, free fatty acids, glucose), a drastic augmentation of hepatic glycogen reserves, and a pronounced increase of total liver weight and liver-somatic index. Constant values of total hepatic DNA showed that liver weight augmentation was not due to cell proliferation, but to a pronounced enlargement of the existing hepatocytes. Major hunger-related structural modifications of carp hepatocytes such as enlarged mitochondria or prominence of the lysosomal compartment were reversed. A significant volume increase of cell nuclei, together with a particularly strong elevation of hepatic RNA concentrations during initial realimentation suggest an immediate stimulation of protein synthesis. Since the cisternae of the endoplasmic reticulum were not reconstituted during that early phase, protein synthesis may have been executed mainly by free ribosomes. With prolonged realimentation, the volume of the endoplasmic reticulum as well as total and relative contents of liver soluble protein continuously increased, whereas RNA concentrations decreased again. An enforcement of liver oxidative capacity was indicated by the augmentation of cellular number and volume of mitochondria. The activities of the enzymes glucose-6-phosphate dehydrogenase and malic enzyme, which convert excess energy into NADPH, increased steadily. Concomitantly, hepatic lipid accumulation was enhanced. In conclusion, liver metabolism during the early recovery phase seems to be dominated both by repair processes and by intensive protein and glycogen synthesis. The liver slows down these processes during prolonged refeeding and directs an increasing percentage of energy and metabolites toward the generation of reducing equivalents and lipid reserves.