Background/Aims: Diabetes mellitus is a disease associated with abnormal carbohydrate metabolism, arising from insulin deficiency and / or malfunction of insulin receptors. The hyperglycemia considered the major causal in the development of chronic clinical complications, like: cataract, retinopathy, nephropathy, neuropathy, generalized microangiopathy and arteriosclerosis. Diabetic neuropathy is the most frequent symptomatic complication of diabetes and potentially one of the most devastating that may result in premature death or loss of limb. It could be caused by glycation of proteins, elevated oxygen free radicals which could damage nerve directly or by inhibiting (nitric oxide) NO synthesis, reducing ATPases activities leading to a defect in nerve function and defective nerve regeneration by impaired synthesis and/or transport of nerve growth factors. Aims of the study: To correlate between some biochemical parameters, changes in electrophysiological study in diabetics with peripheral neuropathy. Methods: 70 subjects were included in this study, 25 were control, 45 were diagnosed as type II (NIDDM) diabetic subjects, divided according to their HbAlc level into (controlled, moderately uncontrolled, uncontrolled diabetics). For each subject: neurological examination; blood aspiration for measurement of (ATPases activities, glutathione level, serum MDA, membrane protein level); nerve conduction study; ophthalmological examination were done. Results and conclusion: Significant increase in HbAlc levels in all uncontrolled diabetic subgroups. HbA1c (glycemic control) is significantly correlated to most of diabetic complications as HbAlc becomes >7.4%. Significant reduction in erythrocyte membrane Na+/K+ , Ca2+ and Mg ATPases activities, and this reduction become more severe as the glycemic control reduced. Reduction in level of erythrocyte reduced glutathione and increased lipid peroxidation shown by increased serum MDA level with more severe changes as the glycemic control reduced. Elevation of erythrocyte membrane protein level in all diabetic subgroups, with more severe increment as the glycemic control reduced. Electrophysiologic parameters are either reduced significantly in diabetic subgroups like (SNCV, MNCV, sensory and motor amplitude), or prolonged as (sensory and motor latency) of median, ulnar, sural and common peroneal nerves, and this defect is increased as the glycemic control reduced.