Recent studies indicated the involvement of arachidonic acid cascade in regulation of
blood glucose. This study was aimed to confirm the involvement of arachidonic acid cascade in the
pathophysiology of diabetes mellitus by assessing the effect of diclofenac, one of the
cyclooxygenase (COX) enzym inhibitors. In dose orientation experiment, mice were divided into
several groups, each was administrated vehicle, diclofenac, or glibenclamide. Blood glucose level
was observed until 240 minutes after drug administration. Optimum dose and administration time
obtained from this experiment was used in the subsequent tests, which consisted of glucose
tolerance test, alloxan diabetes test, glucose tolerance test in alloxan-treated mice, and
antagonistic activity against hyperglicemic factor. Diclofenac at l0 mg/kg bw suppressed blood
glucose elevation in the first 30 minutes after its administration. Despite no improvement observed
in glucose tolerance test under normal condition, diclofenac suppressed glucose level increase in
glucose tolerance in alloxan-treated mice. Furthermore, diclofenac blocked exacerbation of
hyperglycemia in alloxan-treated mice. However, diclofenac did not inhibit epinephrine- induced
blood glucose elevation. Diclofenac at l0 mg/kg bw tended to show antihyperglicemic rather than
hypoglicemic effect. This result indicated the involvement of
arachidonic acid cascade in the pathophysiology of diabetes mellitus.
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