Diabetic neuropathy. Human and experimental.
Human diabetic neuropathy consists of various clinical syndromes and it is unlikely that any single aetiological process is responsible for all of them. There is probably a complex interaction of different metabolic factors, microvascular disease, and perhaps even a genetic predisposition and other as yet unidentified environmental factors. Abnormalities of sorbitol and myo-inositol metabolism have been described in animal models and human studies of neuropathy and must be regarded as of major importance, especially since they can be profoundly influenced by blocking the enzyme aldose reductase. However, a comparison of the abnormalities in the peripheral nervous system of animals with diabetes and in human diabetic neuropathy shows that the clinical and pathological resemblances are not close. Therefore, caution is needed when using the results of animal studies to interpret the manifestations of diabetic neuropathy in man.
D000818:Animals; D001342:Autonomic Nervous System Diseases / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009431:Neural Conduction; D009468:Neuromuscular Diseases / Q000503:physiopathology; D010525:Peripheral Nerves / Q000473:pathology / Q000503:physiopathology; D012677:Sensation