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Trafficking of ENaC...
Trafficking of ENaC subunits in response to acute insulin in mouse kidney
- Article/chapterEnglish2007
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American Physiological Society,2007
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-104059
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-104059URI
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https://doi.org/10.1152/ajprenal.00447.2006DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Studies done in cell culture have demonstrated that insulin activates the epithelial sodium channel (ENaC) via a variety of mechanisms. However, to date, upregulation of ENaC in native renal tissue by in vivo administration of insulin has not been demonstrated. To address this, we injected 6-mo-old male C57BL/CBA mice (n = 14/group) intraperitoneally with vehicle or 0.5 U/kg body wt insulin and examined short-term (1-2 h) sodium excretion and kidney ENaC subunits (alpha, beta, and gamma) and serum and glucocorticoid-induced kinase (SGK-1) regulation. Insulin resulted in a significant reduction in urine sodium (by approximately 80%) that was restored by intraperitoneal administration of the ENaC antagonist, benzamil (1.4 mg/kg body wt). Differential centrifugation followed by Western blotting of whole kidney revealed significantly increased band densities (by 26-103%) for insulin- relative to vehicle-treated mice for alpha- and gamma-ENaC in the homogenate (H), and plasma membrane-enriched fraction (MF), with no difference in the vesicle-enriched fraction (VF). Similarly, beta-ENaC was significantly increased in MF (by 45%) but no change in the H. It was, however, significantly decreased in the VF (by 28%) with insulin. In agreement, immunoperoxidase labeling demonstrated relatively stronger apical, relative to cytosolic, localization of alpha-, beta-, and gamma-ENaC with insulin, whereas, with vehicle, labeling was fairly evenly dispersed throughout collecting duct principal cells. Furthermore, Western blotting showed insulin increased SGK-1 (by 75%) and phosphorylated-SGK band densities (by 30%) but only in the MF. These studies demonstrate novel in vivo regulation of renal ENaC activity and subunit proteins and SGK-1 by insulin in the acute time frame in the mouse.
Subject headings and genre
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epithelial sodium channel
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SGK-1
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hyperinsulinemia
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MEDICINE
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MEDICIN
Added entries (persons, corporate bodies, meetings, titles ...)
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Nordquist, Lina,1977-Uppsala universitet,Integrativ Fysiologi,Nordquist(Swepub:uu)linor172
(author)
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Halagappa, Veerendra K Madala
(author)
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Ecelbarger, Carolyn A
(author)
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Uppsala universitetIntegrativ Fysiologi
(creator_code:org_t)
Related titles
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In:American Journal of Physiology - Renal Physiology: American Physiological Society293:1, s. F178-F1850363-61271522-14661931-857X
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