5
Views
27
CrossRef citations to date
0
Altmetric
Original Article

Aminoguanidine, An Inhibitor of Nitric Oxide Formation, Fails to Protect Against Insulitis and Hyperglycemia Induced by Multiple Low Dose Streptozotocin Injections in Mice

&
Pages 311-314 | Received 23 Nov 1992, Accepted 29 Apr 1993, Published online: 07 Jul 2009
 

Abstract

It has been suggested that pancreatic β-cell destruction occurring during the process leading to insulin-dependent diabetes mellitus (1DDM) involves formation of nitric oxide (NO). We have presently studied the effect of aminoguanidine (AG), which has recently been reported to inhibit generation of NO induced by the cytokine interleukin-1β. AG currently counteracted IL-1β induced impairment of the glucose oxidation rate in rat pancreatic islets. Then we studied the effect of AG on the development of hyperglycemia and pancreatic insulitis in mice treated with multiple low dose injections of streptozotocin (40 mg/kg body-weight for five consecutive days). It was found that one daily intraperitoneal injection of AG (50 mg/kg body-weight) for 14 days failed to prevent the development of diabetes as well as insulitis following the streptozotocin injections. Furthermore, the mice treated with streptozotocin plus AG showed an increased mortality compared to mice treated with streptozotozin plus saline. Although the present data do not exclude a role for NO in IDDM, it raises concerns about the use of testing AG as therapeutic agent in IDDM.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.