Electron Microscopic Studies of the Pancreatic Islets and Some Other Organs in Experimental Congenital Diabetic Rats

Abstract

Nineteen rats were obtained by the mating of two spontaneous diabetic males, that had diabetes for over one month, with three nondiabetic females, all of which were born from alloxan diabetic rats in the same successive generations. General observations on these animals and light and electron microscopic studies on their pancreatic islets as well as some other organs were performed. Among 19 rats, 11 developed diabetes spontaneously without any treatment, 5 of which showed long persistent diabetes.(a) Before the onset of diabetes, the pancreatic B-cells showed hypoplasia (reduced in number and size). Electron microscopically, some B-cells in the granular stage showed degranulation and an increased number of ribosomes, some B-cells in the predominantly agranular stage irregular dilatation of granular endoplasmic reticulum. (b) After the onset of diabetes, some pancreatic B-cells showed hydropic degeneration and vacuolar formation, other B-cells pyknosis and atrophy. Under electron microscopy, marked degranulation, swelling and vacuolation of mitochondria, and a decreased number of ribosomes were observed in all pancreatic B-cells, and in addition, marked irregular dilatation of granular endoplasmic reticulum in the predominantly agranular stage. The adrenal gland showed slight hypertrophy and in the cells of the fascicular zone an increased number of ribosomes and abundant dilated agranular endoplasmic reticula both before and after the onset of diabetes were observed.In the kidney, the glomerulus showed no obvious changes, but the renal tubules demonstrated deposition of glycogen particles in the diabetic stage and they did not show any degenerative lesions in their organelles. In short, in experimental congenital diabetic rats, the pancreatic B-cells work excessively to maintain the animals free of diabetes, during the early prediabetic stage; however, with the aging process their growth disturbance becomes severe, they are exhausted and show degeneration and finally spontaneous diabetes occurs. The presumed hyperfunction of their adrenal cortex accelerates the onset of diabetes.Since Okamoto (1952) found hypoplasia of the pancreatic B-cells in the descendants of alloxan diabetic rabbits, many investigations on these animals have been made, with many interesting results. That is, the diabetic animals (rabbits, rats and guinea pigs) in which diabetes was induced by the administration of alloxan or other diabetogenic substances, were mated after being kept diabetic for more than one month, to obtain F1 offspring and this process was repeated to obtain F2 and several subsequent genrations. On examination it was revealed that these descendants had hypoplasia of the pancreatic B-cells (reduced in number and in size), increased percentage of acidophiles in the adenohypophysis and hypertrophy of the adrenal cortex (especially zona fasciculata). These changes gradually