ENDOCRINE PANCREAS IN EARLY ALLOXAN DIABETES - INCLUDING STUDY OF ALLOXAN INHIBITORY EFFECT OF FEEDING AND SOME HEXOSES

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 85  (2) , 219-229
Abstract
Starved animals [mice and gerbils] were sensitive to alloxan, whereas a more or less inhibitory effect towards alloxan was observed in fed animals, and in starved animals pretreated with glucose, mannose or fructose, but not in those pretreated with galactose. Islets of starved controls possessed larger .beta.-cell mitochondria than those of fed ones. The earliest .beta.-cell changes in the alloxan-treated animals were localized to the mitochondria which showed swelling and disruption of inner and occasionally outer membranes. Later, many mitochondria were disintegrated, and the endoplasmic reticulum and Golgi complex disorganized. Secretory granules were preserved, although sometimes with atypical configuration, in degenerating but non-necrotic .beta.-cells, suggesting that insulin stored in granules is not released until the cells are necrotic. Finally, frank necrosis was seen in some .beta.-cell, whereas others were unaffected. The Ca2+-precipitation studied by pyroantimonate technique and X-ray analysis differed in the .beta.-cells of alloxan-treated animals and in the controls; the former animals exhibited no or only sparse precipitation in mitochondria and secretory granules, but a rich precipitation in the cytoplasmic ground substance, whereas the precipitation in the controls mainly was localized to mitochondria and secretory granules. The primary site of alloxan action in the .beta.-cells is probably localized to the mitochondria.