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J Neurosci Res ; 40(1): 138-44, 1995 Jan 01.
Article in English | MEDLINE | ID: mdl-7714922

ABSTRACT

Neuropathy is an enigmatic and debilitating complication of diabetes. A consensus as to the pathogenesis of this disorder has yet to emerge. Recently, it has been found that the insulin-like growth factors (IGFs) regulate peripheral nerve regeneration, and IGF content is reduced in various diabetic tissues. We tested herein the hypothesis that IGF administration can prevent or ameliorate the impairment of sensory nerve regeneration in streptozotocin diabetic rats. Miniosmotic pumps released small local doses of IGF-I from a catheter routed near a site of sciatic nerve crush or larger systemic doses of IGF-I or IGF-II from a distant subcutaneous site. Whether administered locally or systemically, IGFs protected against the impairment of sensory nerve regeneration. Surprisingly, this protection was obtained despite unabated hyperglycemia. Therefore, the neuropathy involving sensory nerve regeneration in diabetes can be ameliorated or prevented by IGF treatment, independently of hyperglycemia.


Subject(s)
Blood Glucose/drug effects , Diabetes Mellitus, Experimental/physiopathology , Somatomedins/physiology , Animals , Hyperglycemia , Insulin-Like Growth Factor I , Insulin-Like Growth Factor II , Nerve Regeneration , Rats , Rats, Sprague-Dawley
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