A B S T R A C T The factors influencing the development of impaired sciatic motor nerve conduction velocity (MNCV) in acute experimental diabetes were examined. Decreased MNCV developed by the 14th day after streptozotocin administration but only in rats which became hyperglycemic. Insulin treatment, begun on day 3, failed to prevent impaired MNCV in diabetic rats in which improved or normal weight gain and a decreased degree of hyperglycemia was induced. However, insulin treatment prevented the development of impaired MNCV in a group of diabetic rats in which the tail vein plasma glucose concentration was never found to exceed 160 mg/dl during days 6 through 14, and in which the mean+SEM of the average plasma glucose concentration for each animal during the same period was 754+18 mg/dl. In normal rats fed diets containing 0.011% or 0.069% free myoinositol (a presumably normal range), sciatic nerve free myoinositol concentrations were 90-and 60-fold higher than those in plasma. On

No abstract

To determine whether basal phosphoinositide turnover plays a role in metabolic regulation in resting rabbit aortic intima-media incubated under steady state conditions, we used deprivation of extracellular myo-inositol as a potential means of inhibiting basal phosphatidylinositol (PI) synthesis at restricted sites and of depleting small phosphoinositide pools with a rapid basal turnover. Medium myo-inositol in a normal plasma level was required to prevent inhibition of a specific component of basal de novo PI synthesis that is necessary to demonstrate a discrete rapidly turning-over 11,3-'4Clglycerol-labeled PI pool. Medium myoinositol was also required to label the discrete PI pool with [1-'4Clarachidonic acid (AA). The rapid basal turnover of this PI pool, when labeled with glycerol or AA, was not attributable to its utilization for polyphosphoinositide formation, and it seems to reflect basal PI hydrolysis. Depleting endogenous free AA with medium defatted albumin selectively inhibits the component of basal de novo PI synthesis that replenishes the rapidly turningover PI pool. A component of normal resting energy utilization in aortic intima-media also specifically requires medium myoinositol in a normal plasma level and a free AA pool; its magntude is unaltered by indomethacin, nordihydroguaiaretic acid, or Ca2+-free medium. This energy utilization results primarily from Na+/ K+ ATPase activity (ouabain-inhibitable 02 consumption), and in Ca2+-free medium deprivation of medium myo-inositol or of free AA inhibits resting Na+/K+ ATPase activity to a similar degree (60%, 52%). In aortic intima-media basal PI turnover controls a major fraction of resting Na+/K+ ATPase activity.

No abstract

Approximately 25 percent of resting energy utilization in isolated nerve endoneurium is inhibited by medium containing defatted albumin and selectively restored by arachidonic acid but is unaffected by indomethacin or nordihydroguaiaretic acid. The same component of energy utilization is inhibited by small decreases in endoneurial myo-inositol, which decrease incorporation of carbon-14-labeled arachidonic acid into phosphatidylinositol. The fraction of the resting oxygen uptake inhibited by ouabain is decreased 40 to 50 percent by a reduced tissue myo-inositol concentration or by defatted albumin. Metabolic regulation by rapid, basal phosphatidylinositol turnover is dependent on the maintenance of normal tissue myoinositol concentrations.