The role of dietary fat and hepatic triglyceride secretion in cancer-induced hypertriglyceridemia.
Growth of Ehrlich ascites carcinoma induces hyperlipemia in mice. In the present study using male Swiss-Webster mice, we examined whether the usual elevations of plasma triglyceride levels in cancerous mice would occur in the absence of dietary fat. Hypertiglyceridemia developed at a similar rate and to a comparable degree in tumerous mice eating a fat-free (58% glucose) diet and in those fed Purina chow. Maximal hyperlipidemia was observed on day 6 or day 8 in tumorous mice fed either diet. To determine whether the endogenous cancer-induced hyperlipidemia was due to hypersecretion of triglycerides by the liver, triglyceride secretion rates were studied 0, 2, 4, 6, 8, 10, and 12 days after tumor inoculation using Triton WR-1339. The secretory rates did not increase prior to or during the development of hypertriglyceridemia in tumorous mice and were not significantly different from those of control mice. On days 10 and 12, triglyceride secretion actually decreased in tumorous mice. Other possible causes for hypertriglyceridemia are discussed in light of the present findings of undetectable differences in triglyceride secretion rates accompanying growth of Ehrlich ascites carcinoma in mice.
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000097:blood / Q000378:metabolism*; D004041:Dietary Fats / Q000378:metabolism*; D006949:Hyperlipidemias / Q000209:etiology*; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D014280:Triglycerides / Q000097:blood / Q000378:metabolism*
D004041:Dietary Fats; D014280:Triglycerides