Because fasting nerve myo-inositol (myo-Ins) is not decreased in patients with diabetes treated conventionally, in whom neuropathy may develop or may have already developed, it seems unlikely that myo-Ins is the metabolic abnormality that initiates diabetic neuropathy, if nerve myo-Ins is not spuriously high during fasting. At 6 weeks after induction of diabetes with streptozotocin in Sprague-Dawley rats, we found that endoneurial glucose, sorbitol, and fructose were substantially increased and myo-Ins was decreased, as reported by others. By use of multiple linear regression to assess the effect of disease condition, time after feeding (1.5, 4, and 20 hours), and duration of diabetes (1,2,6, and 12 weeks) on nerve sugars and alcohol sugars, for nerve glucose, sorbitol, and fructose only disease condition was a statistically significant factor. For nerve myo-Ins, disease group (control or diabetic rats) (P = 0.08), duration of diabetes (P = 0.02), time after feeding (P<0.001), duration × time (P = 0.01), group × duration (P = 0.03), and group × time (P = 0.05) were significant variables. Because nerve myo-Ins was lower at 20 hours than at 1.5 or 4 hours after feeding, for all durations of diabetes, one can infer that in human nerve the lowest nerve myo-Ins, not high values, occurs in the fasting state. Therefore, one would not expect to find lower nerve myo-Ins levels in human diabetics at times other than the fasting condition.
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