The respiratory metabolism of regenerating rat liver.

Regenerating liver is commonly used as a source of rapidly growing tissue, since the maximum rate of growth of this tissue exceeds that of most tu mors (1, 11). Generally, it has been considered that, in the case of regenerating liver, rapid tissue growth occurs at the expense of unchanged oxygen consumption or glycolysis and that the over-all metabolic patterns of resting adult and regenerat ing liver are essentially the same (3, 8). This con cept arose apparently from a single report (14) concerning the respiratory metabolism of regener ating liver, in which it was concluded that partial hepatectomy had no effect on either the oxygen consumption or the glycolysis of rat liver. The additional energy requirements associated with any rapid growth of a tissue must be satisfied either by an increase in tissue respiration or an in crease in glycolysis. A tissue possessing adequate cytochrome reserve (17) could satisfy any addi tional energy requirements by an increased oxida tion. In the case of the tumor, which is known to be deficient in the cytochrome system and hence possesses no oxidative reserve (9), the energy re quirements are met by an increased glycolysis. It is known that there is a depression in a number of oxidative enzymes in the liver following partial hepatectomy. These enzymes include succinic dehydrogenase (15, 18), malic dehydrogenase, cyto chrome reducÃ-ase, oxalacetic oxidase (15), and glutamic dehydrogenase (7). On the other hand, Greenstein (10) and Shack (17) have reported that the cytochrome oxidase activity in regenerating liver at 48 hours after partial hepatectomy is ap proximately the same as that of normal liver, while Crandall and Drabkin (5) have shown that regenerating liver is not deficient in cytochrome c. It seems probable, therefore, that regenerating liver could respond to the demand for additional energy requirements by an increased tissue res piration. * This research was supported in part by the Atomic Energy Commission, Contract AT-(40-1)-1665.