PREPUBERTAL HYPERGLYCEMIA CAUSES NERVE DAMAGE. |[dagger]| 538

It has been reported that prepubertal duration of diabetes has a minimal influence on the later risk of diabetic complications. Rats made hyperglycemic at 6 weeks of age (before puberty) manifest reduced nerve conduction velocity(NCV) by 10 weeks of age and show morphologic differences in the sciatic tibial nerve after 5 months of hyperglycemia when compared to age matched controls. Fiber diameter, myelin width, and the number of large myelinated fibers (> 6.5 um) were decreased. The number of small (< 6.5 um) developing myelinated fibers were increased. Rats made hyperglycemic at 26 weeks of age (post pubertal) had elevated glycosylated hemoglobin and sciatic nerve sorbitol but maintained normal NCVs and had little change in morphology after 7 months of hyperglycemia. Thus, animals with maturing peripheral nerve structure and function (characteristic of the prepubertal period) exposed to chronic hyperglycemia manifest greater pathologic alterations than occur when more mature nerves are exposed to similarly elevated glucose concentrations for an even greater duration. This suggests that growing maturing tissues of prepubertal children may be more sensitive to the toxic effects of hyperglycemia than mature adult tissues. In summary, the tissues of prepubertal animals are not immune to the toxic effects of hyperglycemia. Blood glucose control is likely to be important for the normal maturation of tissues in prepubertal children with diabetes mellitus.