Dietary control of lipogenesis in vivo in host tissues and tumors of mice bearing Ehrlich ascites carcinoma.

We have determined rates of fatty acid (FA) synthesis from glucose carbon and all two-carbon units in control mice and in mice bearing Ehrlich ascites carcinomas. Using [U-14C]glucose and 3H2O as tracers under three nutritional conditions (24-hr fasted, 24-hr fasted-refed, and ad libitum fed-refed), we found that lipogenic regulatory mechanisms in adipose tissue and livers of mice bearing advanced tumors were similar to those of control mice. FA synthesis from glucose carbon and from all two-carbon units in livers of tumorous (8-day tumors) mice was at least as fast as that in control mice in the fasted and fasted-refed states but only about one-half that of controls in the fed-refed condition. The rate of FA synthesis from two-carbon units in carcasses of mice with 8-day tumors was not significantly different from that of controls in any of the 3 dietary states studied; however, in fed-refed mice with 8-day tumors, the rate of FA synthesis in the whole body was only one-half that of controls. The rate of FA synthesis from glucose carbon in carcasses of these tumorous mice was significantly depressed compared to that of controls in both the 24-hr-fasted and the fed-refed states. In well-nourished mice with early (5-day) tumors, the whole-body lipogenic rate from all two-carbon units was not depressed. Thus, decreased lipogenesis observed in host tissues of mice with advanced tumors is due to malnourishment; this secondarily depressed lipogenic activity probably contributes significantly to the loss of body fat that may occur at later stages of tumor growth. De novo FA synthesis in Ehrlich ascites cells, although small compared to that of the whole-body rate, was substantial in relation to lipids needed for tumor nutrition.