Changes in the rates of lipogenesis and hepatic triglyceride secretion in mice bearing Ehrlich ascites carcinoma

The growth of Ehrlich ascites tumors (EAT) in mice induces hypertriglyceridemia and depletion of lipid stores. H-Riop: Swiss mice in early and late stages of tumor growth were examined to investigate whether an increase in liver synthesis of fatty acids (FA) and/or an increase in the liver triglyceride (TG) secretion rates (TGSR) would contribute to endogenous cancer-induced hypertriglyceridemia. Using 3H2O as tracer, FA synthesis decreased in the liver of tumorous animals. Hepatic TGSR also decreased during the development of hypertriglyceridemia. On the basis of these results, hypertriglyceridemia is probably not due to hyperproduction of lipids by the liver. In the late stage of tumor growth a considerable drop of FA synthesis also ensued in the adipose tissues, which probably participated in the loss of carcass lipids. At the early stage of tumor growth FA synthesis in the EAT cells was substantial in relation to the low lipid content of these cells, but in the late period FA synthesis slowed down, indicating that the triglyceride-rich "older" tumor cells obtained a large part of their lipids performed by the host.