Pain in diabetes is a common debilitating condition for which pathophysiolo
gy remains poorly understood. To evaluate the underlying mechanisms, we use
d intravenous injection of streptozotocin to produce rapid (24-hour) onset
of diabetes (blood glucose > 300 mg/dL and urine glucose > 2,000 mg/dL with
polyuria). In this model, mechanical and thermal hyperalgesia and tactile
allodynia are detectable by 48 hours after streptozotocin administration in
the absence of ketonuria or physical debility. Treatment with insulin atte
nuated hyperglycemia and prevented the development of mechanical and therma
l hyperalgesia. Direct application of streptozotocin to peripheral nerve di
d not produce hyperalgesia. We conclude that streptozotocin can induce pain
independent of a general debility or direct toxic effect of streptozotocin
on peripheral nerve and that elevated blood glucose may contribute to the
enhanced nociception. (C) 2001 by the American Pain Society.