Abstract

Diabetes mellitus was produced in rats by the administration of streptozotocin and observations made over a period of 2 months. Four groups of animals were studied: onset and end controls, untreated diabetic rats and rats treated daily with a long-acting insulin preparation. Body weight increased in the end controls and insulin-treated diabetic animals to a similar degree over the observation period but was reduced in the untreated diabetic rats. Skeletal growth, assessed by measurements of tibial length, was also reduced in the untreated diabetic rats and partially corrected by insulin treatment. Myelinated fibre diameter in the tibial and sural nerves increased over the observation period in the controls, but the increase was less in the untreated animals and the growth deficit was not corrected by insulin treatment. Myelinated fibre numbers did not alter in the tibial or sural nerves between the onset and end controls. Numbers were significantly less in the tibial nerves of both the untreated and insulin-treated diabetic rats as compared with the two control groups; in the sural nerves, fibre numbers did not differ significantly between the four groups. Finally, the number of degenerating axons, assessed in teased fibre preparations, was very small in the control and untreated diabetic animals but was significantly increased in the insulin-treated group. Measurements of plasma glucose concentrations did not suggest that the axonal degeneration could be related to hypoglycaemia. The explanation for this paradoxical effect of insulin therapy is uncertain. It may be dependent upon fluctuations in blood glucose levels or other metabolic actions of insulin apart from its hypoglycaemic effect.

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