The complications of chronic diabetes affect many systems including the nervous system wherein the peripheral neuropathy is the most common presenting feature and which if not controlled may necessitate limb amputation. Since the exact mechanism of hyperglycemia-induced peripheral neuropathy and its treatment are not completely known, the present study was aimed at an effort to further the information in this regard. After ethical clearance, 36 animals were divided into six groups having six rats each. The groups consisted of age-matched controls and experimental groups of two weeks, one month, two months, four months and six months duration of diabetes. Diabetes was induced by a single dose of streptozotocin (60 mg/kg, intraperitoneal). At the end of each experimental period, animals were euthanized and perfusion fixed with Karnovsky’s fixative. The blood serum was subjected to biochemical analysis and the sciatic nerve tissue blocks were processed for paraffin sectioning, routine and special staining for light microscopy. Biochemical, histomorphological findings and histopathological features revealed that the prolonged duration of hyperglycemia resulted in the raised serum creatinine, lowered serum total protein, reduction of myelinated fibers and remarkable thickening of endoneurial, perineurial and epineurial collagen. It is concluded that the biochemical alterations, change in the ratio of myelinated fibers and heaping up of collagen fibers at every level of organization appear to be important contributing factors for the deterioration of peripheral nerve functions in chronic diabetes.
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