Alloxan Diabetes
It is an experimental diabetes mellitus produced in animals by the administration of alloxan, which damages the insulin-producing islet cells of the pancreas. Alloxan is a well-known and universally used agent for evoking experimental diabetes through its toxic effect on the B cells of the Langerhans islets.
Alloxan Cause Diabetes
The uric acid derivative initiates free radical damage to DNA in the beta cells of the pancreas, causing the cells to malfunction and die. When these beta cells fail to operate normally, they no longer produce enough insulin, or in other words, they cause one variety of adult-onset type 2 diabetes. Alloxan's harmful effects on the pancreas are so severe that the Textbook of Natural Medicine calls the chemical "a potent beta-cell toxin." However, even though the toxic effect of alloxan is common scientific knowledge in the research community, the FDA still allows companies to use it when processing foods we ingest. eptozotocin action, B cells undergo the destruction by necrosis.
The Effect of Alloxan Diabetes on Rabbits
Our experimental results find no direct application to the problem of arterial disease in human diabetes. It was not dependent on the sex or weight of the animal, nor upon the daily dosage of cholesterol, the form in which it was administered, nor the duration of cholesterol feeding. In the course of the experiment it was demonstrated that the inhibitory effect was apparent in cholesterol-fed diabetic rabbits whether or not their diet was supplemented with vegetable oil. A comparison was made of the effects of cholesterol feeding in normal rabbits and in rabbits rendered patiently diabetic by means of alloxan. Only two factors were observed to be consistently associated with the inhibition of the expected morphological effects of cholesterol feeding, namely, the diabetic state and a degree of visible lipemia considerably greater than that observed in the control animals. In view of the inhibitory effect on the development of experimental cholesterol atherosclerosis observed in alloxan-diabetic rabbits, the effect of alloxan diabetes on the retrogression of such arterial lesions was studied in another series of experiments. No effect on retrogression could be demonstrated within periods lasting up to a maximum of approx. 5 months after the cessation of cholesterol feeding.
The results of our two series of experiments, considered together, indicate that the process of deposition of lipids in the arterial walls is governed by factors different from those that are operative in the process of removal of lipids after they have been deposited. The inhibition of the development of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits must depend on interference with the process of deposition of lipids and not on a process of removal of lipids as fast as they are deposited. The inhibitory effect observed in these experiments would appear to depend upon some as yet undetermined factor or factors implicit in the diabetic state or closely associated with it. The experimental data presented demonstrate clearly that hypercholesterolemia is not the sole factor concerned in the genesis of experimental cholesterol atherosclerosis, but that gross or histological evidence of a morphological basis for the inhibitory effect either in the aorta or in the other organs in which it was observed.