Lipid metabolism in
hormone-dependent (HD) GR mouse mammary
tumors was compared to that in
hormone-independent (HI)
tumors and normal mammary tissues. HD
tumors, like normal mammary tissue but unlike HI
tumors, synthesized medium-chain-length
fatty acids (MCFA). However, when treated with
hormones (
estrone and
progesterone), the HI
tumors were induced to produce MCFA. The activity of
thioesterase II correlated positively with the synthesis of MCFA and was influenced by the
hormones administered. The activities of
NADP+-linked
malate dehydrogenase,
citrate lyase,
acetyl-CoA carboxylase, and
fatty acid synthetase, although lower in
tumors than in normal glands, were not different in HD as compared to HI
tumors. Whereas the predominating
lipids synthesized in normal glands were
triglycerides,
phospholipids comprised about half of the
lipid synthesized in the
tumors, with no difference between HD and HI
tumors. The conversion of D-[U-14C]
glucose to 14CO2 was higher in HD
tumors than in HI
tumors but increased in HI
tumors treated with
hormones in vivo. By a comparison of the 14CO2 produced from D-[1-14C]
glucose and from D-[6-14C]
glucose in the presence and absence of an electron acceptor (
methylene blue), it was demonstrated that regeneration of NADP+ from
NADPH was a rate-limiting step for the pentose phosphate pathway in the
tumors. Hence, while differences in the lipid metabolism can be demonstrated between HD and HI GR mouse mammary
tumors, some of the changes are due to the
hormone treatment rather than to a specific alteration in the
tumor itself.