Increase of the Gluconeogenic and Decrease of the Glycolytic Capacity of Rat Liver with a Change of the Metabolic Zonation after Partial Hepatectomy

Abstract

During the first 72 h after 67% partial hepatectomy of female Wistar rats (160 g) the specific activities [.mu.mol .times. min-1 .times. (g liver)-1] of the glucogenic glucose-6-phosphatase (EC 3.1.39.) and fructosebisphosphatase (EC 3.1.3.11) and of the glycolytic hexokinase (EC 2.7.1.1) and 6-phosphofructokinase (EC 2.7.1.1) remained essentially constant. However, the activity of the glycolytic pyruvate kinase (EC 2.7.1.40) (L-plus M2-type) was decreased slightly and that of glucokinase (EC 2.7.1.2) was decreased markedly to below 30%, while the glucogenic phosphoenolpyruvate carboxykinase (EC 4.1.1.32) was increased to over 200%. Between 10 and 40 h after partial hepatectomy, when the proliferation started in the periportal area, a shift of the glucogenic glucose-6-phosphatase-rich zone from its normal periportal to an intermediate or even perivenous position was observed histochemically. After 48 h, when the proliferation was no longer restricted to the periportal zone, the normal glucose-6-phosphatase zonation (as before partial hepatectomy) was restored. Glycogen was degraded rapidly during the first 4 h after operation; it was later repeatedly resynthesized and degraded in correlation with the feeding rhythm of the animals. The zonation of glycogen metabolism was in accord with the observed zonation of glucose-6-phosphatase. The considerable increase of the glucogenic over the glycolytic capacity is necessary because the 1/3 liver remnant, during the postabsorptive phase, must provide the same amount of glucose for utilization by the CNS and the erythrocytes as provided by the intact liver before partial hepatectomy. The transient shift of the glucose-6-phosphatase-rich zone within the parenchyma indicates that the proliferating hepatocytes in the periportal zone probably become glycolytic so that the quiescent cells in the neighboring zone must take over the glucogenic function.