Influence of streptozotocin-induced diabetes on myelinated nerve fibre maturation and on body growth in the rat

Influence of streptozotocin-induced diabetes on myelinated nerve fibre maturation and on body growth in the rat

A. K. Sharma;S. Bajada;P. K. Thomas;A. K. Sharma;S. Bajada;P. K. Thomas;
acta neuropathologica 1981 Vol. 53 pp. 257-265
234
sharma1981actainfluence

Abstract

Observations were made between the ages of 2 and 12 months on rats made diabetic with streptozotocin at the age of 1 month, and compared with the findings in age-matched controls. Tibial length and body weight in the control animals increased progressively over the period examined, the growth rate being more rapid in the initial stages. Both of these parameters were consistently less in the diabetic animals over the whole of the observation period. Myelinated fibre numbers and diameters were measured in the tibial and plantar nerves. In the tibial nerve, fibre diameter did not differ between the diabetic and control animals up until 4 months of age; thereafter it changed little in the diabetic animals, but continued to increase in the controls. The findings in the medial plantar nerve were more difficult to analyse but showed comparable although less pronounced changes; fibre diameter may be have diminished in the diabetic nerves after 6 months. Teased fibre studies demonstrated few abnormalities in the tibial nerve, either in the control or the diabetic rats. In the lateral plantar nerves, there was a significant excess of axonal degeneration and regeneration in the diabetic nerves. It was concluded that diabetes impairs growth in nerve fibre diameter, but only after 4 months of age. Before then, no growth retardation is obvious, despite the fact that tibial length and body weight are less. This suggests that the peripheral nervous system may be protected against growth retardation during the early part of the postnatal growth period. The significance of the axonal degeneration in the plantar nerves is uncertain, but it may represent either an increased vulnerability of diabetic nerve to compression injury or, less probably, a distal axonopathy related to the diabetic state.

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