Diabetes mellitus was first produced experimentally in dogs by von Mering and Minkowski in 1889 by means of total extirpation of the pancreas. G. F. Young in 1937 produced diabetes in dogs by daily injection of extracts of anterior pituitary for a period of several weeks. Dunn, Sheehan and McLetchie,1 while attempting to elucidate the pathogenesis of the crush syndrome, administered alloxan to various animals in an effort to establish tubular nephritis. Many animals died during the first day. Investigation of these deaths revealed acute necrosis of the islet tissue of the pancreas. The development of this lesion was accompanied by an initial rise of the blood sugar, followed by intense hypoglycemia; they believed that the lesion was caused by overstimulation of the islets with overproduction of the insulin and later death of the cells by overstrain. Jacobs2 first described the initial hyperglycemic and hypoglycemic phases following intravenous
DIABETES DUE TO ALLOXAN. JAMA. 1948;138(12):891–892. doi:10.1001/jama.1948.02900120033011
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