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Abstract
Objectives. To examine the effects of inhibition of cyclooxygenase (COX) on islet hormone secretion in vitro and on pancreatic islet blood flow in vivo.Methods. Insulin release was measured in a static incubation system of islets isolated from Wistar-F rats after inhibition of COX-1 and COX-2 with SC 560 (COX-1), FR 122047 (COX-1), rofecoxib (COX-2), or indomethacin (both COX-1 and COX-2). In other rats organ blood flow values were measured with a microsphere technique during both normo- and hyperglycemia after administration of these enzyme inhibitors.Results. Serum insulin values were lower after pretreatment with a COX-1 inhibitor or a non-selective COX inhibitor in both control and glucose-injected rats in vivo, whereas COX-2 inhibition had no such effects. However, inhibition of COX had only minor effects on insulin release in vitro. Inhibition of COX affected neither total pancreatic nor islet blood flow in normoglycemic rats. Hyperglycemia caused an increase in both these flow values and in the duodenum. The increase in total pancreatic and duodenal blood flow was prevented by inhibition of COX-2 or non-selective COX inhibition. However, no effects on islet blood flow were seen after COX inhibition.Conclusion. Inhibition of COX affects insulin release and blood glucose concentrations in vivo. However, COX inhibition has only minor effects on pancreatic islet blood flow, but prevents the glucose-induced increase in total pancreatic blood flow.
Highlights
Arachidonic acid can be modified by three major pathways, namely cyclooxygenase (COX), lipoxygenase, and cytochrome P450 into biologically active eicosanoids
Basal insulin release at 1.67 mmol/L glucose was similar in all groups, besides islets pretreated with indomethacin, where a lower value was seen
Glucose increased insulin release in all groups when compared with basal values, but this response was potentiated by inhibition of COX-1 by either SC
Summary
Arachidonic acid can be modified by three major pathways, namely cyclooxygenase (COX), lipoxygenase, and cytochrome P450 into biologically active eicosanoids. These substances have many biological activities, e.g. influencing smooth muscle contraction, platelet aggregation, and inflammatory responses [1,2,3]. The present study focuses on COX, which converts arachidonic acid into various prostaglandins [4]. COX is present in two isoforms of which COX-1 is constitutively expressed in most cells at a constant level, whereas COX-2 is constitutively expressed in the brain and spinal cord. In most cells COX-2 expression is induced by pro-inflammatory cytokines and growth factors [1]
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