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The
th Annual Meeting of March 10-11, 2018 The Endocrine Society and The Diabetes Association of the R.O.C. (Taiwan)
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THE ROLE OF PGE2 METABOLISM IN THE PATHOGENESIS OF DIABETIC KIDNEY DISEASE CHIH-HUNG LIN Department of Internal Medicine, National Taiwan University Hospital, Taipei City, Taiwan
Diabetic kidney disease (DKD) is one of the most common complications of diabetes. The pathogenesis is very sophisticated, involving many unique albeit inter-correlated cell types and mechanisms. Despite the efforts and recent progress in treating diabetes, deterioration of renal function is still inevitable in certain patients. Such condition emphasizes the necessity of further investigation of this disease. Prostaglandins (PGs) play important parts in the maintenance of homoeostasis and the pathogenesis of various diseases. Many studies have proposed the roles of different PGs in the pathogenesis of DKD. As the major renal metabolite, PGE2 seems to have both protective and hazardous effects on the kidney via different EP receptors. On the contrary, knowledge about the effect of metabolism of PGE2 on DKD is still very limited. PGE 2 is a mediator with short half-life. It is catabolized by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) into 15-keto-PGE2, followed by prostaglandin reductase 2 (PTGR2), which further catalyzes 15-keto-PGE2 into 13,14-dihydro-15-keto-PGE2. Little is known about the pathophysiological functions of these PGE2-catabolizing enzymes. One intriguing fact is that the metabolites of PG might have reno-protective potential. Thus, the aim of the present study is to elucidate the role of PGE2 metabolism in the pathogenesis of DKD. By manipulating the expression of PTGR2, its effects on various phenotypes of DKD are examined.
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