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PubMed1954

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. IV. The effect of insulin therapy on the inhibition of atherosclerosis in the alloxan-diabetic rabbit.

Experiments were undertaken to ascertain whether the previously demonstrated inhibition of the development of experimental aortic atherosclerosis in alloxan-diabetic rabbits fed cholesterol was due to the injection of alloxan per se or to the existence of the diabetic state produced by alloxan. It was established that, by treating the diabetic state with insulin, the diabetic state could be ameliorated and the inhibitory effect obviated. It was therefore concluded that the inhibitory phenomenon was not due to the injection of alloxan per se but that it was associated with one or more factors that characterize the alloxan diabetic state in the rabbit and that are reversible by insulin therapy. 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. The previously reported metabolic abnormalities of the diabetic animals were confirmed. It was established that suitable treatment of the cholesterol-fed diabetic animals with insulin would bring all the metabolic aberrations, including those of the serum lipids, into reasonably close correspondence with those observed in non-diabetic rabbits fed cholesterol.

Alloxan↗
PubMed1958

Activation of quiescent mucormycotic granulomata in rabbits by induction of acute alloxan diabetes.

In normal rabbits subcutaneous granulomata produced by the injection of a spore suspension of Rhizopus oryzae remained confined to the site of inoculation, showed no fungus proliferation, no longer yielded the agent on culture 10 weeks after inoculation, and eventually healed. Similar well established granulomata in rabbits with acute alloxan diabetes induced 8, 10, and 15 days after injection of the fungus uniformly showed activation of the infection. This occurred only in animals showing acetonuria. In these animals the skin lesions showed proliferation of the fungus frequently associated with invasion and early necrosis of the granuloma wall. In some instances, spread of the infection to adjacent tissues with invasion of blood vessels had occurred. These experiments illustrate that changes in host metabolism can activate a preexisting quiescent infection.

Animals↗
PubMed1959

The development of the acute inflammatory response to experimental cutaneous mucormycosis in normal and diabetic rabbits.

The histologic changes associated with the development of the acute inflammatory response to experimental cutaneous mucormycosis were studied at various times from 5 minutes to 24 hours after inoculation into normal rabbits and in rabbits with acute alloxan diabetes and acidosis. In normal animals the response by polymorphonuclear leukocytes began within a few minutes after inoculation, increased rapidly in extent and intensity and reached its peak within 6 to 12 hours. By that time there was also early proliferation of fibroblasts and of large mononuclear cells and these cellular reactions, together with the accumulated granulocytes, began to produce a demarcation of the lesions. Beginning 4 to 6 hours after inoculation the fungus showed some growth but this remained confined to the necrotic center of the lesions. In the diabetic rabbits the onset of the response by polymorphonuclear leukocytes was delayed by several hours, reduced in intensity and was apparently less effective. There was no proliferation of fibroblasts and the lesions were spreading rather than circumscribed. Fungus growth in the tissues began shortly after inoculation, was marked, progressed rapidly, and soon extended beyond the site of inoculation. The large mononuclear cells, however, appeared at about the same time and in equal number in the lesions of both diabetic and non-diabetic animals and showed no morphologic changes. It is concluded that a significant delay and impaired effectiveness of the response by polymorphonuclear leukocytes, a lack of fibroblastic proliferation and an enhanced growth of the fungus lower host resistance to infection with it and are directly consequent on severe alterations in host metabolism.

Animals↗
PubMed1954

The mechanism of alloxan protection in experimental atherosclerosis.

Experiments were performed to compare the effects of cholesterol feeding in (a) control rabbits, (b) alloxan-diabetic rabbits, and (c) rabbits injected with alloxan while the pancreas was temporarily occluded from the circulation. The alloxan-diabetic rabbits consumed significantly higher quantities of cholesterol and food and had serum cholesterol and lipoprotein (S(f) 5-9 and S(f) 16-30) concentrations significantly increased over the control levels. They failed to show a commensurate increase in the degree of atherosclerosis. Rabbits in which the diabetogenic action of alloxan was prevented by temporary occlusion of the pancreas from the circulation during its administration developed grades of hypercholesterolemia, hyperlipoproteinemia, and atherosclerosis not significantly different from the controls. The results are interpreted as indicating that the effects of alloxan on tissues other than the pancreas do not protect against experimental atherosclerosis produced by cholesterol feeding.

Alloxan↗