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Influence of the Hereditary Obese-Hyperglycemic Syndrome and of Alloxan Diabetes on the Survival of Mice with Ehrlich Ascites Carcinoma^*

Jo'Ann Jehl, Jean Mayer and Ralph W. McKee

( Department of Nutrition, Harvard School of Public Health, Boston, Mass., and Department of Physiological Chemistry, University of California, School of Medicine, Los Angeles, Calif.)

1. Mice with the hereditary obese-hyperglycemic syndrome survived significantly longer than control nonobese animals when given injections intraperitoneally of Ehrlich mouse ascites carcinoma cells.

2. C57BL mice with induced alloxan diabetes survived significantly longer than the control nondiabetic mice when injected intraperitoneally with Ehrlich mouse ascites carcinoma cells.

3. The results are discussed in light of the fact that the hereditarily obese-hyperglycemic mice have an increased rate of lipogenesis from acetate even when food intake is limited and show hormonal imbalance; and in view of the preliminary findings that the Ehrlich mouse ascites tumor cells from alloxan diabetic mice have a lowered acetate metabolism and an increased alanine decarboxylation.

^* Supported in part by grants-in-aid from: National Institute of Arthritis and Metabolism (A-49), National Institutes of Health, Public Health Service, Bethesda; Sugar Research Foundation, New York; Nutrition Foundation, New York; and J. M. Kaplan Foundation, Inc., New York. That part of the work that was done at the University of California was supported in part by the Institute of Cancer Research, United States Public Health Service, Bethesda.

Present address: Department of Physiological Chemistry, University of California, School of Medicine, Los Angeles, Calif.

Received 3/14/55.