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Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone.

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Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone. / Rexhepaj, Rexhep; Rotte, Anand; Kempe, Daniela S; Sopjani, Mentor; Föller, Michael; Gehring, Eva-Maria; Bhandaru, Madhuri; Gruner, Ivonne; Mack, Andreas F; Rubio-Aliaga, Isabel; Nässl, Anna-Maria; Daniel, Hannelore; Kuhl, Dietmar; Lang, Florian.

in: PFLUG ARCH EUR J PHY, Jahrgang 459, Nr. 1, 1, 2009, S. 191-202.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Rexhepaj, R, Rotte, A, Kempe, DS, Sopjani, M, Föller, M, Gehring, E-M, Bhandaru, M, Gruner, I, Mack, AF, Rubio-Aliaga, I, Nässl, A-M, Daniel, H, Kuhl, D & Lang, F 2009, 'Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone.', PFLUG ARCH EUR J PHY, Jg. 459, Nr. 1, 1, S. 191-202. <http://www.ncbi.nlm.nih.gov/pubmed/19672619?dopt=Citation>

APA

Rexhepaj, R., Rotte, A., Kempe, D. S., Sopjani, M., Föller, M., Gehring, E-M., Bhandaru, M., Gruner, I., Mack, A. F., Rubio-Aliaga, I., Nässl, A-M., Daniel, H., Kuhl, D., & Lang, F. (2009). Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone. PFLUG ARCH EUR J PHY, 459(1), 191-202. [1]. http://www.ncbi.nlm.nih.gov/pubmed/19672619?dopt=Citation

Vancouver

Rexhepaj R, Rotte A, Kempe DS, Sopjani M, Föller M, Gehring E-M et al. Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone. PFLUG ARCH EUR J PHY. 2009;459(1):191-202. 1.

Bibtex

@article{7bdc2024a9ac434b8e8d448842b668e7,
title = "Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone.",
abstract = "According to recent in vitro experiments, the peptide transporter PepT2 is stimulated by the serum- and glucocorticoid-inducible kinase SGK1. The present study explored the contribution of SGK1 to the regulation of electrogenic intestinal peptide transport. Intestinal PepT1 was expressed in Xenopus oocytes, and peptide transport was determined by dual electrode voltage clamping. Peptide transport in intestinal segments was determined utilizing Ussing chamber. Cytosolic pH (pH( i )) was determined by BCECF fluorescence and Na(+)/H(+) exchanger activity was estimated from Na(+)-dependent pH recovery (pH ( i )) following an ammonium pulse. In PepT1-expressing Xenopus oocytes, coexpression of SGK1 enhanced electrogenic peptide transport. Intestinal transport and pH( i ) of untreated mice were similar in SGK1 knockout mice (sgk1 ( -/- )) and their wild-type littermates (sgk1 ( +/+ )). Glucocorticoid treatment (4 days 10 microg/g body weight (bw)/day dexamethasone) increased peptide transport in sgk1 ( +/+ ) but not in sgk1 (-/-) mice. Irrespective of dexamethasone treatment, luminal peptide (5 mM glycyl-glycine) led to a similar early decrease of pH( i ) in sgk1 (-/-) and sgk1 (+/+) mice, but to a more profound and sustained decline of pH( i ) in sgk1 (-/-) than in sgk1 ( +/+ ) mice. In the presence and absence of glycyl-glycine, pH ( i ) was significantly enhanced by dexamethasone treatment in sgk1 ( +/+ ) mice, an effect significantly blunted in sgk1 ( -/- ) mice. During sustained exposure to glycyl-glycine, pH ( i ) was significantly larger in sgk1 (+/+) mice than in sgk1 (-/-) mice, irrespective of dexamethasone treatment. In conclusion, basal intestinal peptide transport does not require stimulation by SGK1. Glucocorticoid treatment stimulates both Na(+)/H(+) exchanger activity and peptide transport, effects partially dependent on SGK1. Moreover, chronic exposure to glycyl-glycine stimulates Na(+)/H(+) exchanger activity, an effect again involving SGK1.",
author = "Rexhep Rexhepaj and Anand Rotte and Kempe, {Daniela S} and Mentor Sopjani and Michael F{\"o}ller and Eva-Maria Gehring and Madhuri Bhandaru and Ivonne Gruner and Mack, {Andreas F} and Isabel Rubio-Aliaga and Anna-Maria N{\"a}ssl and Hannelore Daniel and Dietmar Kuhl and Florian Lang",
year = "2009",
language = "Deutsch",
volume = "459",
pages = "191--202",
journal = "PFLUG ARCH EUR J PHY",
issn = "0031-6768",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Stimulation of electrogenic intestinal dipeptide transport by the glucocorticoid dexamethasone.

AU - Rexhepaj, Rexhep

AU - Rotte, Anand

AU - Kempe, Daniela S

AU - Sopjani, Mentor

AU - Föller, Michael

AU - Gehring, Eva-Maria

AU - Bhandaru, Madhuri

AU - Gruner, Ivonne

AU - Mack, Andreas F

AU - Rubio-Aliaga, Isabel

AU - Nässl, Anna-Maria

AU - Daniel, Hannelore

AU - Kuhl, Dietmar

AU - Lang, Florian

PY - 2009

Y1 - 2009

N2 - According to recent in vitro experiments, the peptide transporter PepT2 is stimulated by the serum- and glucocorticoid-inducible kinase SGK1. The present study explored the contribution of SGK1 to the regulation of electrogenic intestinal peptide transport. Intestinal PepT1 was expressed in Xenopus oocytes, and peptide transport was determined by dual electrode voltage clamping. Peptide transport in intestinal segments was determined utilizing Ussing chamber. Cytosolic pH (pH( i )) was determined by BCECF fluorescence and Na(+)/H(+) exchanger activity was estimated from Na(+)-dependent pH recovery (pH ( i )) following an ammonium pulse. In PepT1-expressing Xenopus oocytes, coexpression of SGK1 enhanced electrogenic peptide transport. Intestinal transport and pH( i ) of untreated mice were similar in SGK1 knockout mice (sgk1 ( -/- )) and their wild-type littermates (sgk1 ( +/+ )). Glucocorticoid treatment (4 days 10 microg/g body weight (bw)/day dexamethasone) increased peptide transport in sgk1 ( +/+ ) but not in sgk1 (-/-) mice. Irrespective of dexamethasone treatment, luminal peptide (5 mM glycyl-glycine) led to a similar early decrease of pH( i ) in sgk1 (-/-) and sgk1 (+/+) mice, but to a more profound and sustained decline of pH( i ) in sgk1 (-/-) than in sgk1 ( +/+ ) mice. In the presence and absence of glycyl-glycine, pH ( i ) was significantly enhanced by dexamethasone treatment in sgk1 ( +/+ ) mice, an effect significantly blunted in sgk1 ( -/- ) mice. During sustained exposure to glycyl-glycine, pH ( i ) was significantly larger in sgk1 (+/+) mice than in sgk1 (-/-) mice, irrespective of dexamethasone treatment. In conclusion, basal intestinal peptide transport does not require stimulation by SGK1. Glucocorticoid treatment stimulates both Na(+)/H(+) exchanger activity and peptide transport, effects partially dependent on SGK1. Moreover, chronic exposure to glycyl-glycine stimulates Na(+)/H(+) exchanger activity, an effect again involving SGK1.

AB - According to recent in vitro experiments, the peptide transporter PepT2 is stimulated by the serum- and glucocorticoid-inducible kinase SGK1. The present study explored the contribution of SGK1 to the regulation of electrogenic intestinal peptide transport. Intestinal PepT1 was expressed in Xenopus oocytes, and peptide transport was determined by dual electrode voltage clamping. Peptide transport in intestinal segments was determined utilizing Ussing chamber. Cytosolic pH (pH( i )) was determined by BCECF fluorescence and Na(+)/H(+) exchanger activity was estimated from Na(+)-dependent pH recovery (pH ( i )) following an ammonium pulse. In PepT1-expressing Xenopus oocytes, coexpression of SGK1 enhanced electrogenic peptide transport. Intestinal transport and pH( i ) of untreated mice were similar in SGK1 knockout mice (sgk1 ( -/- )) and their wild-type littermates (sgk1 ( +/+ )). Glucocorticoid treatment (4 days 10 microg/g body weight (bw)/day dexamethasone) increased peptide transport in sgk1 ( +/+ ) but not in sgk1 (-/-) mice. Irrespective of dexamethasone treatment, luminal peptide (5 mM glycyl-glycine) led to a similar early decrease of pH( i ) in sgk1 (-/-) and sgk1 (+/+) mice, but to a more profound and sustained decline of pH( i ) in sgk1 (-/-) than in sgk1 ( +/+ ) mice. In the presence and absence of glycyl-glycine, pH ( i ) was significantly enhanced by dexamethasone treatment in sgk1 ( +/+ ) mice, an effect significantly blunted in sgk1 ( -/- ) mice. During sustained exposure to glycyl-glycine, pH ( i ) was significantly larger in sgk1 (+/+) mice than in sgk1 (-/-) mice, irrespective of dexamethasone treatment. In conclusion, basal intestinal peptide transport does not require stimulation by SGK1. Glucocorticoid treatment stimulates both Na(+)/H(+) exchanger activity and peptide transport, effects partially dependent on SGK1. Moreover, chronic exposure to glycyl-glycine stimulates Na(+)/H(+) exchanger activity, an effect again involving SGK1.

M3 - SCORING: Zeitschriftenaufsatz

VL - 459

SP - 191

EP - 202

JO - PFLUG ARCH EUR J PHY

JF - PFLUG ARCH EUR J PHY

SN - 0031-6768

IS - 1

M1 - 1

ER -