Metabolic abnormalities in diabetic peripheral nerve: relation to impaired function.
An hypothesis is presented relating several well-defined metabolic abnormalities in diabetic peripheral nerve to impaired peripheral nerve function by a sodium-potassium ATPase mechanism. It is proposed that this hypothesis be tested in the most well-defined animal model for human insulin deficiency diabetes currently available--the BB diabetic rat.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D004734:Energy Metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism; D007294:Inositol / Q000378:metabolism; D008297:Male; D010525:Peripheral Nerves / Q000201:enzymology / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D010725:Phosphocreatine; D007294:Inositol; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose