Abstract
The islets of Langerhans in the obese homozygous mutant (ob/ob) saline-control mice were markedly increased in the size and total cell numbers over those of lean controls. There was marked degranulation of B-cells, but with still present β-granules in some cells, enlarged swollen mitochondria, vesicular endoplasmic reticulum, dilated Golgi, and the presence of many tightly-bound secretory granules. There were many lysosomes and much osmiophilic material (probably lipid) in many B-cells. A-cells showed slight degranulation and dilated endoplasmic reticulum. Six weeks after a single dose ofalloxan, there was degranulation and increased numbers of tightly-bound granules, swollen mitochondria, minimal dilatation of endoplasmic reticulum, and many lipid bodies and lysosomes in B-cells. Six weeks after administration ofstreptozotocin, there was marked degranulation of many cells, with some persisting β-granules, markedly vesiculated and dilated rough endoplasmic reticulum, swollen degenerating mitochondria, and many tightly-bound granules in B-cells. Degenerative changes were present in occasional A-cells, characterized by empty vacuoles and dilated endoplasmic reticulum. The presence of numerous membrane-bound vesicles, many immature β-granules and proliferations of Golgi and endoplasmic reticulum indicate attempt at recovery of function in the streptozotocin-treated obese mouse. However, the association of numerous empty endoplasmic cysts and vesicles and the persisting significantly fewer B-cells, as compared with saline- or alloxan-treated obese mice (p⩽0.05), points to lack of recovery from the toxic insult after six weeks. Islet hyperplasia and degranulation, accompanied by evidence of accelerated formation of secretion products of B-cells, as well as enlarged bizarre mitochondria, are anatomic support for accelerated insulin turnover as a response of the islets of Langerhans of the obese mouse to an insulin stimulatory factor. A-cell changes were probably secondary to hyperglycemia.
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