1, 5-Anhydroglucitol (AG) is decreased in the serum of poorly controlled diabetic patients. Although the metabolism of AG is largely unknown, the low serum AG concentration of the patients has been attributed to the increased urinary excretion of AG in association with glycosuria. In order to clarify the effects of impaired renal function on the metabolism of AG, we measured both serum and urinary AG concentrations in 28 non-diabetic patients with renal disease (RD group) who had no glycosuria in association with various degrees of decreased glomerular filtration rate (GFR). Serum AG concentrations were decreased in the RD group even in the absence of glycosuria. The degree of decrease in serum AG level was correlated with the reduction in GFR. No correlation was observed in diabetic patients with glycosuria. Urinary excretion of AG appeared to be increased in the RD group based on their low serum AG level. These results suggest that the low serum concentrations of AG in patients with chronic renal failure may be caused, at least partly, by an increase in the urinary excretion of AG.
We have reported that the vasotropic agent, prostaglandin E1 analogue OP1206·α-CD (OP) ameliorates the decrease in sciatic motor nerve conduction velocity (MCV) and Na+/K+-ATPase activity of rats with streptozocin-induced diabetes without normalizing abnormal nerve sorbitol or myo-inositol content. This observation suggests that nerve Na+/K+-ATP-ase activity may be regulated by unknown metabolites other than myo-inositol. In order to examine this possibility, the effect of OP on Na+/K+-ATPase activity was examined in vitro. Twenty-seven 8-week-old Sprague-Dawley rats were used in the experiment. Diabetes mellitus was induced by intravenous injection of streptozocin 45 mg/kg. Six weeks after the injection, the diabetic rats had significantly higher levels of plasma glucose, lower body weights and slower sciatic motor nerve conduction velocities than the control rats (all p<0.001). Sciatic nerves isolated six weeks after treatment were incubated with various concentrations of OP: the decreased Na+/K+-ATPase activity was ameliorated in a dose-dependent manner, and the improvement was significant at concentrations higher than 0.5ng/ml in the diabetic rats. Nerve cAMP concentrations were also increased in a dose-dependent manner in the diabetic rats. These rasults suggest that OP has a direct effect on diabetic nerve tissue via a mechanism which might be associated with an increase in nerve cAMP levels rather than a vasotropic action.