Abstract：
:The overproduction of the free radical nitric oxide (NO) by activated immunocompetent cells with subsequent development of local oxidative stress is supposed to be one of the possible pathophysiological mechanisms of beta-cell damage during streptozotocin-induced diabetes. The blockade of increased NO production by simultaneous administration of NO-synthase inhibitors partially suppresses the hyperglycemia and the increase of glycated hemoglobin concentration. Here we summarize the current state of knowledge concerning the modulation of streptozotocin-induced diabetes development by treatment with NO-synthase inhibitors including the partial inhibition of the changes in serum leptin levels. The differences in the reaction to streptozotocin administration between wild type mice and inducible NO-synthase knockout mice are also discussed. The overproduction of NO during the development of streptozotocin-induced diabetes is probably an important part of the complex autoimmune reaction which leads to the destruction of pancreatic beta-cells. Further clarification of the role of nitric oxide in streptozotocin-induced diabetes development could have important clinical implications.
journal_name
Physiol Resjournal_title
Physiological researchauthors
Haluzík M,Nedvídková Jsubject
Has Abstractpub_date
2000-01-01 00:00:00pages
S37-42eissn
0862-8408issn
1802-9973journal_volume
49 Suppl 1pub_type
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