Insight on the Metabolic Pathogenesis of Diabetic Peripheral Neuropathy in Sciatic Nerves of Streptozotocin Diabetic Rats
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Peripheral neuropathy is the most common and perhaps the most devastating complication associated with diabetes mellitus. Many theories regarding the pathogenesis of diabetic peripheral neuropathy has been proposed. The present study was designed to investigate the problem of the pathogenesis of diabetic peripheral neuropathy. Thirty male albino rats were made diabetic by streptozotocin intravenous injection (65 mg/kg) and another thirty rats were used as a control group. Sciatic nerves were surgically removed from both diabetic and control rats and were used for the estimation of glucose, pyruvate, lactate, ATP, fructose, sorbitol and myoinositol. Plasma levels of sodium, potassium, glucose, lactate, acetoacetate fi-hydroxy butyrate and osmolality were also measured. In the diabetic sciatic nerves, after 4 weeks of the induction of diabetes, there were significant increases (P<0.001) in glucose, fructose and sorbitol compared to controls. While after 24 weeks of diabetes, the diabetic sciatic nerves showed significant increases in glucose, fructose 1,6- bisphosphate, fructose, sorbitol (P<0.001), lactate and ATP (P<0.05) compared to controls. In the diabetic rats, after 4 and 24 weeks of the induction of diabetes, there were significant increases in the plasma levels of glucose, 0-hydrant butyrate, acetoacetate (P<0.001) and plasma osmolality (P<0.05) compared to control rats. While after 24 weeks of diabetes, the diabetic rats showed significant increases in. the plasma levels of potassium (P<0.05) and lactate (P<0.001) compared to the control rats. So, we could conclude that the metabolic abnormalities combine to produce deleterious changes that make a major contribution to the etiology of diabetic peripheral neuropathy. The present study suggests that fructose and sorbitol accumulation with the osmotic desequilibrium and nonenzymatic glycation of macromolecules by fructose contribute to the mechanism of diabetic peripheral neuropathy.