Journal of Lipid Research, Vol. 9, 337-341, May 1968
Copyright © 1968 by Lipid Research, Inc.

Lack of adaptation in lipogenesis by hepatoma 9121

J. C. Elwood and Harold P. Morris

Department of Biochemistry, Upstate Medical Center, State University of New York, Syracuse, New York 13210, and the National Cancer Institute, National Institutes of Health, Public Health Service, Bethesda, Maryland 20014

The "minimal deviation" hepatoma 9121, implanted in rats, was shown to biosynthesize fatty acids from acetate-1-¹⁴C at the same rate as normal rat liver but faster than host liver. Feeding the host animals a fat-deficient diet caused fatty acid biosynthesis to be increased 3- to 13-fold in liver, but the dietary regimen did not influence fatty acid biosynthesis in the tumor tissue.

Oxygen consumption and the oxidation of acetate and mevalonate to CO₂ were all affected by the dietary manipulation in liver but not in hepatoma. The fat-deficient diet decreased incorporation of acetate and mevalonate into cholesterol by the liver of control animals, increased it in the liver of host animals, and had no effect on this process in hepatoma. Thus, the transplantable tumor has lost the adaptive power of its parent tissue to respond to the dietary stimulus.

The changes in fatty acid composition in total lipids in response to the fasting and refeeding were also markedly different in hepatoma from those in liver of the host animals. These results support the concept that this tumor is characterized by a loss of some metabolic controls.

Supplementary key words lipogenesis • cholesterol biosynthesis • adaptive • liver • hepatoma • fat-deficient diet • tumor • linoleate accumulation • rat

Submitted on January 23, 1968
Accepted on February 2, 1968

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