A HISTOLOGICAL STUDY OF THE PANCREAS, LIVER AND KIDNEY BOTH DURING AND AFTER RECOVERY FROM ALLOXAN DIABETES1

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Abstract
One hundred and eighty two hamsters were injected intravenously, via the ocular sinus, with a diabetogenic dose of alloxan. Their blood sugars were determined by an anthrone technique at intervals for a period of 30 weeks. Samples of the organs were taken under Nembutal anesthesia during various periods of the diabetic phase and from time to time after recovery. Tissues were fixed in Bouin''s, Flemming''s and a saturated solution of picric acid in absolute alcohol and stained in: modified aldehyde fuchsin; gallocyanin chrome alum and periodic acid-Schiff with and without maltase digestiou. The islets of alloxan diabetic hamsters return to normal either by: recuperation of cells damaged or inhibited by the drug; by proliferation from small ducts; by transformation of acinar tissue. Intermittent and persistent diabetics recover thaough the latter mechanisms. In most cases, a return to physiological normal precedes that of histological normal by several weeks. During hyperglycemia, the livers of persistent and intermittent diabetics show less stored glycogen but these return to normal concomitant with the fall in blood sugar. The R.N.A. content of the livers of severe diabetics is likewise reduced in hyperglycemia and also returns to normal with recovery. Cast formation in the kidney as well as periportal flbrosis and focal necrosis of the liver occur among untreated animals, their incidence increasing with age. Alloxan may aggravate such conditions but is not necessarily the cause. Diabetogenic doses of alloxan do not result in fatty metamorphosis of the liver but do: increase the size and number of lipid droplets situated at the periphery of hepatic cords; induce the release of lipids from the cords to be subsequently engulfed by Kupffer cells. Alloxan does not appear to be causally related to lipids found in or near fibrotic or necrotic areas.