Aplastic carcinoma in diabetic mice: hyperglycemia-suppressed proliferation rate and insulin synthesis by tumor cells.
Increased glucose levels in blood of diabetic and of normoinsulinemic hyperglycemic CBA/H mice were accompanied by suppressed growth of aplastic carcinoma. Tumors maintained in diabetic mice grew faster after each subsequent transplantation into diabetic mice, but those maintained in hyperglycemic normoinsulinemic mice grew at a constant rate. Evidence revealed that tumor growth was suppressed by hyperglycemia. The observed proliferation enhancement of aplastic carcinoma maintained in diabetic mice was caused by de novo insulin synthesis, probably by the tumor cells themselves.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002455:Cell Division; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism; D007328:Insulin / Q000096:biosynthesis*; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008808:Mice, Inbred CBA
D001786:Blood Glucose; D007328:Insulin