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Dietary lipids, in particular unsaturated fat, promote the development of many experimental tumors. However, no mechanisms to fully explain these effects have been elucidated. Recent reports, which we summarize here, suggest a role for gap junction-mediated intercellular communication in the process of tumor promotion. We also review tumor-promoting effects of dietary fat on experimental, particularly mammary, carcinogenesis. Our main focus is to review recent data examining the inhibitory effects of unsaturated fatty acids on metabolic cooperation in Chinese hamster V79 cells. These data suggest that inhibition of junctional communication may be involved mechanistically in the promotion of tumors by high levels of dietary unsaturated fat. Finally, potential mechanisms by which unsaturated fatty acids inhibit metabolic cooperation are examined.

The incorporation of 1-(14)C-Acetate into tissue cholesterol of the baboon was measured. Using this indicator gray matter of the cerebrum indicated greater metabolic activity than did white matter.Other tissues besides neural tissue were examined. The peak of radioactivity occurred between 3 and 4 hr. The highest incorporation of radioactivity was measured in the adrenal gland. Liver, spleen and kidney values were of intermediate order.

Glucose-1 and glucose-6 labeled with tritium or carbon-14 were incorporated in vivo into brain and liver sterol. Differential incorporations of glucose labeled in both positions were compared. A higher than expected incorporation of C-1 from glucose was noted.

The appearance of methyl esters of fatty acids in lipid extracts was studied. Experimental evidence indicates that these esters are both natural components of tissues as well as products of technical manipulation. Effect of temperature on the latter process was studied. The results of these experiments show that the post-mortem increase of fatty acid methyl esters could best be explained by postulating an enzymatic rather than a chemical process.