Glucose-induced alterations in nerve metabolism: current perspective on the pathogenesis of diabetic neuropathy and future directions for research and therapy.
Recent animal and in vitro studies have identified several interrelated metabolic abnormalities in diabetic nerve that are attributable to elevated ambient glucose concentrations. In combination, these metabolic changes may induce a variety of biochemical and biophysical alterations in peripheral nerve that are highly relevant to the pathogenesis of diabetic neuropathy. This article reviews the current status of several of these metabolic defects and describes ways in which their interaction could lead to pathogenetically important changes in nerve metabolism, function, and structure. Areas of related future research are also discussed.
Greene
D A
DA
Lattimer
S
S
Ulbrecht
J
J
Carroll
P
P
D000818:Animals; D001693:Biological Transport, Active; D003925:Diabetic Angiopathies / Q000150:complications; D003929:Diabetic Neuropathies / Q000209:etiology* / Q000378:metabolism / Q000628:therapy; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D007294:Inositol / Q000378:metabolism; D008954:Models, Biological; D009431:Neural Conduction; D009474:Neurons / Q000378:metabolism*; D012106:Research; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013012:Sorbitol / Q000378:metabolism
D007294:Inositol; D013012:Sorbitol; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose