title: Ganglioside treatment of genetic and alloxan-induced diabetic neuropathy.
abstract: Peripheral neuropathy is a common complication of diabetes. Using the mutant diabetic mouse C57BL/ks (db/db) and alloxan-treated rats, 30 days after intoxication, we investigated development and treatment with gangliosides of such a disease. The db/db mouse develops a neuropathy characterized by a loss in conduction velocity shown as early as 80-90 days after birth and maintained throughout life. At later stages (5-6 months of age) there is a drop in slow transport and myelin particle density. These changes are correlated by a lack of response to insulin treatment, which, prior to this stage, is capable of improving nerve conduction velocity (NCV). On the other hand gangliosides became effective, improving NCV, myelin particle density and sensory perception (auditory deficit) at 5 months of age in the db/db mouse. We presume that this differential neuronal response to insulin and gangliosides indicates a change of the neuropathy from a metabolic stage to neuronal. Alloxan induced diabetic neuropathy is treatable with gangliosides even 30 days after intoxication.
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000161:Acoustic Stimulation; D000818:Animals; D001370:Axonal Transport; D001369:Axons / Q000502:physiology; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D005072:Evoked Potentials, Auditory / Q000187:drug effects; D005614:Freeze Fracturing; D005732:Gangliosides / Q000494:pharmacology*; D051379:Mice; D008817:Mice, Mutant Strains; D009121:Muscle Denervation; D009186:Myelin Sheath / Q000648:ultrastructure; D009416:Nerve Regeneration / Q000187:drug effects; D012584:Sciatic Nerve / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D005732:Gangliosides; D000110:Acetylcholinesterase