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논문분류	춘계학술대회 초록집
제목	Diabetic condition is associated with decreased αklotho expression and re-localization of sodium-phosphrous cotransporter (Napi2a/2c) in the kidney.
저자	Jinho Lee* 1, Hyo Jin Kim2, Kyung Don Ju1, Bodokhsuren Tsogbadrakh1, Kook-Hwan Oh1
출판정보	2016; 2016(1):
키워드	aklotho, diabetic nephropathy, phosphorus metabolism
초록	Background: Diabetic nephropathy (DN) is the leading cause of the chronic kidney disease (CKD) all over the world. α-klotho, as an antiaging protein, is mainly expressed in the kidney. α-klotho is a major regulator of mineral metabolism and is deranged in the CKD. Here, we explored αklotho expression in diabetic condition (in vivo and in vitro), and how this change in αklotho could affect phosphorus metabolism. Methods: We extracted the kidneys from 15-week-old mice (C57BL6 db/db) and analyzed αklotho expression via immunohistochemistry assay. db/m mice were used as control. In addition, we analyzed α-klotho and sodium-phosphrous cotransporter (Napi2a/2c) expression from S1 proximal tubule cells (immortalized) of the wild-type C57BL6 mice after treatment with normal glucose (5mM, NG) or high glucose (30mM, HG) by confocal microscopy. Results: Immunohistochemistry exhibited significantly decreased expression of α-klotho from db/db mouse kidney, as compared with control. In vitro, HG treated cells expressed remarkably lower level of αklotho. HG treatment caused re-localization of Napi2a/2c molecules toward the cell membrane, which is the main action site of sodium-phosphorus cotransporter. Conclusion: Our results indicate that renal α-klotho decreases in diabetic conditions. Napi2a/2c was re-localized to the cell membrane after high glucose treatment. Our current study will continue to seek for mechanistic links between high glucose, αklotho and renal phosphorus regulation. Table:
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