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Table of Contents
36, No. 1, 2012
Issue release date: February 2013
Section title: Original Paper
Kidney Blood Press Res 2012;36:320-334
(DOI:10.1159/000343390)

Fructose Acutely Stimulates NHE3 Activity in Kidney Proximal Tubule

Queiroz-Leite G.D.a · Crajoinas R.O.b · Neri E.A.a · Bezerra C.N.A.a · Girardi A.C.C.b · Rebouças N.A.a · Malnic G.a
aDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, bHeart Institute (InCor), Medical School, University of São Paulo São Paulo, Brazil
email Corresponding Author

Gabriella Duarte Queiroz-Leite

Department of Physiology and Biophysics, Institute of Biomedical Sciences

University of São Paulo, Av. Prof. Lineu Prestes, 1524, São Paulo, 05508-900 SP (Brazil)

Tel. +55-11-3091-7280, Fax +55-11-3091-9922, E-Mail gabidq@icb.usp.br

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Abstract

Background/Aims: Fructose causes a sodium-sensitive hypertension and acutely reduces the urinary Na+ excretion, suggesting that it may regulate the activity of renal tubular sodium transporters. NHE3 is highly expressed in proximal tubule (PT), along with proteins that mediate fructose transport and metabolism. The present work was outlined to investigate whether fructose modulates proximal NHE3 activity and to elucidate the molecular mechanisms underlying this modulation. Methods/Results: Using in vivo stationary microperfusion, we observed that fructose stimulates NHE3 mediated JHCO3- reabsorption. The MAPK pathway is not involved in this activation, as demonstrated by using of MEK/MAPK inhibitors, whereas experiments using a PKA inhibitor suggest that PKA inhibition plays a role in this response. These results were confirmed in vitro by measuring the cell pH recovery rate after NH4Cl pulse in LLC-PK1, a pig PT cell line, which showed reduced cAMP levels and NHE3 phosphorylation at serine-552 (PKA consensus site) after fructose treatment. Conclusions: NHE3 activity is stimulated by fructose, which increases proximal tubule Na+ reabsorption. The molecular mechanisms involved in this process are mediated, at least in part, by downregulation of the PKA signaling pathway. Future studies are needed to address whether fructose-stimulated NHE3 activity may contribute to renal injury and hypertension.

© 2012 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: November 12, 2012
Published online: December 12, 2012
Issue release date: February 2013

Number of Print Pages: 15
Number of Figures: 0
Number of Tables: 0

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

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