Neuropathic Diabetics Research Articles

Oxygen uptake kinetics during exercise in diabetic neuropathy.

To assess the effect of autonomic and sensorineural dysfunction on O2 uptake kinetics, we studied the exercise response of seven diabetic humans having peripheral sensory and cardiac autonomic neuropathy, eight diabetics without neuropathy, and eight normal subjects. Maximal O2 uptake (VO2max), ventilatory anaerobic threshold, and O2 uptake kinetics were assessed. Metabolic control was optimized 12 h prior to and during testing by intravenous insulin infusion. Patients with diabetic neuropathy had a reduced VO2max [83 +/- 6% predicted vs. 104 +/- 6% (nonneuropathic diabetics) and 107 +/- 5% (normals); P less than 0.05]. However, there was no difference in ventilatory anaerobic threshold [14.8 +/- 0.9 (neuropathic diabetics) vs. 18.0 +/- 1.0 (nonneuropathic diabetics) and 16.7 +/- 1.5 ml O2.kg-1.min-1 (normals); P greater than 0.25]. The phase I increment in O2 uptake (VO2) and estimated cardiac output and the time constant of VO2 during constant-load exercise at 40% VO2max also were similar in all groups. We propose that the instantaneous increase in VO2 and cardiac output at exercise onset in diabetes with impaired neurogenic reflexes is caused primarily by mechanical and metabolic events in exercising muscle that cause venous compression and vasodilation.

Diminished Flare Response in Neuropathic Diabetic Patients: Comparison of Effects of Substance P, Histamine, and Capsaicin

The flare response in skin largely depends on an intact primary sensory fiber, the C-fiber. We measured the flare response to the intradermal injection of substance P, histamine, and capsaicin in control subjects and in diabetic patients with and without clinically obvious polyneuropathy. The neuropathic diabetic patients had a reduced flare response to substance P, histamine, and capsaicin, compared with control and nonneuropathic diabetic subjects. The smaller flare response in the neuropathic diabetics after capsaicin administration suggested a dysfunction of the peripheral component of the C-fiber. Alternatively, dysfunction of the mast cell or vascular reactivity may contribute to the diminished flare. Because C-fibers participate in nociception in addition to the flare response, the findings of this study, by a method that permits a quantifiable measurement of the function of peripheral sensory neurons in diabetic subjects, has potential usefulness in evaluating sensory neuropathy in diabetic patients.

Dietary myo-inositol intake and peripheral nerve function in diabetic neuropathy

The effect of variations in dietary myo-inositol intake upon plasma myo-inositol concentrations, urinary myo-inositol excretion, motor nerve conduction velocities in the median and peroneal nerves, and sensory nerve conduction velocities in the median and sural nerves was studied in six nondiabetic subjects and in twenty patients with symptomatic distal symmetrical diabetic polyneuropathy. Diets were developed which provided either a low, a normal, or a high intake of myo-inositol. In control subjects, the low- myo-inositol diet was found to decrease, while the high- myo-inositol diet increased both the preprandial plasma myo-inositol concentrations and the daily urinary excretion of myo-inositol. These diets had little effect upon measured nerve function in the control subjects, although the high- myo-inositol diet appeared to slightly reduce the median sensory nerve conduction velocity in this group. In the neuropathic diabetics, the low- and high- myo-inositol diets were found to have similar effects upon the plasma myo-inositol concentrations and urinary myo-inositol excretion, but did not affect the plasma glucose concentrations. When analyzed by groups, no statistically significant changes were observed in any of the measured nerve conduction velocities in the diabetic patients. However, when the change in nerve conduction velocity was analyzed, it was found that the ingestion of the high- myo-inositol diet resulted in a statistically significant increase in the median sensory (+1.92 m/sec, p < 0.001) and the sural sensory nerve conduction velocity (+6.67 m/sec, p < 0.001). In contrast, ingestion of the low- myo-inositol diet produced a statistically significant decrease in the median motor (−2.35 m/sec, p < 0.001) and the peroneal motor nerve conduction velocity (−1.18 m/sec, p < 0.001). Thus, ingestion of a diet enriched in myo-inositol may have a salutory effect upon peripheral nerve function in the patient with symptomatic diabetic neuropathy and appears to be without significant side effects in this patient group.

Mechanisms regulating renin release.

Mechanisms regulating renin release.