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Title: Fructose as a modulator of proximal tubule (PT) H plus transport
Authors: QUEIROZ-LEITE, Gabriella DuarteCRAJOINAS, Renato O.NERI, Elida A.BEZERRA, Camila N. A.GIRARDI, Adriana C. C.REBOUCAS, Nancy A.MALNIC, Gerhard
Citation: FASEB JOURNAL, v.26, 2012
Abstract: High fructose (F) intake adversely affects the kidneys. This study was outlined to investigate F effects on NHE3 activity. Microperfusion showed that 2 and 3mM F stimulate JHCO3-(nmol/cm2 x s) (2.87 ± 0.19, P < 0.001 and 2.78 ± 0.14, P < 0.01 x 2.08 ± 0.10, control). Action of F on S3226 (NHE3 inhibitor) sensitive-component showed NHE3 stimulation (1.18 ± 0.07 x 1.81 ± 0.01, P < 0.0001). MAPK pathway is not involved in this activation, as demonstrated by using U1026 and SB203580 (MEK and p38 MAPK inhibitors), whereas 8 br cAMP (cAMP analogue) and forskolin (phosphodiesterase inhibitor) + IBMX (adenylyl cyclase activator) showed that PKA inhibition plays a role in this response. F stimulated JH+ (mM/min) after an acid pulse in LLC-PK1, a pig PT cell line (11.44 ± 1.09 3mM F x 5.98 ± 0.82 control, P < 0.01). HOE694 (NHE1 inhibitor) and S3226 showed that F increases NHE3, not NHE1 activity. Signaling pathways investigation showed similar results in PT and LLC-PK1. Cells were treated or not with F for 5, 15 and 30 min and the ATP and cAMP contents were examined. There was a significant decrease in ATP (47, 53 and 37%, respectively) and in cAMP (45 and 31%, respectively) and a not significant reduction at 30 min. Antibody against phosphorylated substrates showed PKA inhibition in F treated cells. Thus, F stimulates NHE3 activity through PKA inhibition, which increases Na+ reabsorption and can contribute to renal injury.
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Comunicações em Eventos - HC/InCor
Instituto do Coração - HC/InCor

Comunicações em Eventos - LIM/13
LIM/13 - Laboratório de Genética e Cardiologia Molecular

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