Abstract
Previous results from our laboratory showed myelinated fiber alterations in the aortic depressor nerve (ADN) from rats rendered diabetic for 15 days (short term). The ultrastructure and the acute effect of insulin treatment, particularly in the unmyelinated fibres of this nerve, were not yet investigated in this experimental model, being the aim of this work. Wistar rats received a single intravenous injection of streptozotocin (STZ – 40 mg/Kg) 15 days (N=7) before the experiments. Control animals (N=7) received vehicle (citrate buffer) and treated animals (n=6) received a subcutaneous injection of insulin (10 IU/Kg) on a daily basis beginning 3 days after the STZ injection. Under pentobarbital anaesthesia the ADNs were isolated and had their spontaneous activity recorded. Afterwards, proximal and distal segments of the nerves were prepared for transmission electron microscopy studies. Morphometry of the myelinated and unmyelinated fibres was carried out with the aid of computer software. Nerves from diabetic animals showed some unmyelinated fiber enlargement with signs of swelling and degeneration, and the Schwann cells mitochondria presented enlargement and clustering formation. On treated animals, an important thickening of the Schwann cells’ basement membrane was present and some myelinated fibers showed thin myelin sheaths. The endoneural blood vessels ultrastrucutre was preserved in all nerves from the three experimental groups. Myelinated axon area and diameter was significantly larger on insulin treated animals, compared to both, controls and acute diabetic groups, on both segments. No other differences were observed between groups for the myelinated or unmyelinated fibers morphometric parameters. Investigation of experimental models of diabetes in early or acute stage of the disease provide relevant information on the physiopathological mechanisms involved in the alterations present in patients with chronic diabetes and its complications. We suggest that insulin treatment alone might have a role on the morphological alterations present in diabetic neuropathy.
Highlights
Diabetes is a metabolic disorder of multiple etiologies caused by defects in insulin secretion, insulin action, or both, resulting in chronic hyperglycemia
Neuropathy is a common complication of diabetes that accounts for a significant high morbidity [1]
Blood glucose level was significantly high on both STZ groups three days after injection compared to controls
Summary
Diabetes is a metabolic disorder of multiple etiologies caused by defects in insulin secretion, insulin action, or both, resulting in chronic hyperglycemia. Initial symptoms such as thirst, polyuria, and weight loss are unspecific and often not severe, or even absent. Comi and Corbo [2] documented that one third of diabetic patients present some degree of neuropathy but a recent publication from the Centers for Disease Control and Prevention [3] indicated that this percent is much higher (up to 70%). Despite recent information about the mechanisms for many of the long term complications of diabetes, the exact pathogenesis of diabetic neuropathy remains unknown
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