A correlation between the capacity of tumor-bearing animals to maintain normal glucose levels and the stimulation of gluconeogenesis from noncarbohydrate sources has been established. Gluconeogenesis was shown to counterbalance the tendency toward hypoglycemia caused by tumors in mice with Crocker sarcoma and Guelstein 22a hepatoma, and in rats with Zajdela ascites hepatoma. Mobilization of liver and muscle glycogen reserve failed to ensure normal glucose levels in rabbits with Brown-Pierce carcinoma.

The enhancement of endogenous glucose formation from 14C-labeled amino acids in the tumor-bearing host depended upon the response to glucocorticoids of the tissues involved in gluconeogenesis. Mice with Ehrlich ascites carcinoma developed severe hypoglycemia that increased with tumor growth. There was no enhancement of gluconeogenesis in these animals.

A prolonged stress imposed on such mice or the administration of large doses of cortisol was found to stimulate gluconeogenesis and elevate the blood glucose concentration to a normal level. A reduced responsiveness of the host's tissues to glucocorticoids is regarded as a manifestation of the systemic action of the tumor on distant organs.

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