Changes in lipoprotein lipase activity (LPLA) in tumor cells and tissues in mice bearing Ehrlich ascites tumor.
Lipid content and lipoprotein lipase activity (LPLA) of serum and various tissues of mice bearing Ehrlich ascites tumor have been studied. The growing tumor caused hyperlipidemia, depletion of adipose tissue, a slight increase of heart lipid content, lipid accretion in the tumor cells and a relative increase of free fatty acids and cholesterol in the ascites fluid. LPLA of the post-heparin plasma was higher in tumorous than in control mice. Tumor growth led to a marked decline of LPLA in the adipose tissue and an elevation in the heart. It declined slightly in the older tumor cells and increased in the ascites plasma of the same. It has been concluded that: a) decline in adipose tissue LPLA may play an important part in the development of hyperlipidemia and loss of body fat; b) increase of the heart LPLA proves insufficient for elimination of the piled up blood lipids during progression; c) LPLA in the ascites fluid may favour the hydrolysis of triglycerides entering the ascites fluid, which might account at least in part for the fatty acids made available to the tumor; d) LPLA detected in the tumor cells might also facilitate the assimilation of lipids by the tumor cells.
D000273:Adipose Tissue / Q000201:enzymology; D000818:Animals; D001202:Ascitic Fluid / Q000201:enzymology; D002286:Carcinoma, Ehrlich Tumor / Q000201:enzymology*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008071:Lipoprotein Lipase / Q000097:blood / Q000378:metabolism*; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D009206:Myocardium / Q000201:enzymology; D014280:Triglycerides / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D008055:Lipids; D014280:Triglycerides; D008071:Lipoprotein Lipase