Diabetic Mice: Hyperglycemia-Suppressed

ABSTRACT-Increased glucose levels in blood of diabetic and of normoinsulinemic hyperglycemic CBA/H mice were accom-panied by suppressed growth of aplastic carcinoma. Tumors maintained in diabetic mice grew faster after each subsequent transplantation into diabetic mice, but those maintained in hyper-glycemic normoinsulinemic mice grew at a constant rate. Evi-dence revealed that tumor growth was suppressed by hypergly-cemia. The observed proliferation enhancement of aplastic car-cinoma maintained in diabetic mice was caused by de novo insu-lin synthesis, probably by the tumor cells themselves.-J Natl Cancer Inst 62: 139-141, 1979. Several phenomena demonstrating links between car-bohydrate metabolism and neoplastic diseases have been reported. Thus many tumors are accompanied by hypoglycemia caused apparently by their intense glu-cose consumption (1-4). Also, many tumors grow much more slowly in diabetic animals than in normal animals. This phenomenon was explained by the lack of insulin (5-7). Maintaining an aplastic carcinoma in diabetic mice, we noted an ever-decreasing survival time of tumor-bearing animals together with an enhanced rate of tumor growth with each passing generation. Here we present evidence that these effects are caused by the appearance of insulin in di~betic a~im~ls a?d t~at aplastic carcinoma cells cultivated In diabetic mrce during several generations release insulin in amounts high enough to raise the concentration of insulin to the normal level. MATERIALS AND METHODS Male CBA/H mice, 12 weeks old, weighing about 21 g, were used. They were kept in groups of 3-5 and were supplied with pelleted food and tap water ad libitum. The primary mammary carcinoma developed spon-taneously in an inbred CBA-T6T6 mouse (Departmen