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Diabetes 53:S190-S192, 2004
© 2004 by the American Diabetes Association, Inc.

Section IV: Lipid Modulators of Islet Function

Glucose-Induced Regulation of COX-2 Expression in Human Islets of Langerhans

Shanta J. Persaud, Chris J. Burns, Véronique D. Belin, and Peter M. Jones

Centre for Reproduction, Endocrinology and Diabetes, King’s College London, London, U.K

Cyclo-oxygenase (COX), the enzyme responsible for conversion of arachidonic acid to prostanoids, exists as two isoforms. In most tissues, COX-1 is a constitutive enzyme involved in prostaglandin-mediated physiological processes, whereas COX-2 is thought to be induced by inflammatory stimuli. However, it has previously been reported that COX-2 is the dominant isoform in islets and an insulin-secreting ß-cell line under basal conditions. We have investigated the relative abundance of COX-1 and COX-2 mRNAs in MIN6 cells, a mouse insulin-secreting cell line, and in primary mouse and human islets. We found that COX-2 was the dominant isoform in MIN6 cells, but that COX-1 mRNA was more abundant than that of COX-2 in freshly isolated mouse islets. Furthermore, COX-2 expression was induced by maintenance of mouse islets in culture, and experiments with human islets indicated that exposure of the islets to hyperglycemic conditions was sufficient to upregulate COX-2 mRNA levels. Given that hyperglycemia has been reported to increase human ß-cell production of interleukin-1ß and that this cytokine can induce COX-2 expression, our observations of glucose-induced induction of COX-2 in human islets suggest that this is one route through which hyperglycemia may contribute to ß-cell dysfunction.

Address correspondence and reprint requests to S. J. Persaud, Room 3.2A, New Hunt’s House, King’s College London, London SE1 1UL, U.K. E-mail: shanta.persaud{at}kcl.ac.uk


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Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2004 by the American Diabetes Association.