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SGK1-sensitive renal tubular glucose reabsorption in diabetes.

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SGK1-sensitive renal tubular glucose reabsorption in diabetes. / Ackermann, Teresa F; Boini, Krishna M; Völkl, Harald; Bhandaru, Madhuri; Bareiss, Petra M; Just, Lothar; Vallon, Volker; Amann, Kerstin; Kuhl, Dietmar; Feng, Yuxi; Hammes, Hans-Peter; Lang, Florian.

in: AM J PHYSIOL-RENAL, Jahrgang 296, Nr. 4, 4, 2009, S. 859-866.

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

Harvard

Ackermann, TF, Boini, KM, Völkl, H, Bhandaru, M, Bareiss, PM, Just, L, Vallon, V, Amann, K, Kuhl, D, Feng, Y, Hammes, H-P & Lang, F 2009, 'SGK1-sensitive renal tubular glucose reabsorption in diabetes.', AM J PHYSIOL-RENAL, Jg. 296, Nr. 4, 4, S. 859-866. <http://www.ncbi.nlm.nih.gov/pubmed/19158347?dopt=Citation>

APA

Ackermann, T. F., Boini, K. M., Völkl, H., Bhandaru, M., Bareiss, P. M., Just, L., Vallon, V., Amann, K., Kuhl, D., Feng, Y., Hammes, H-P., & Lang, F. (2009). SGK1-sensitive renal tubular glucose reabsorption in diabetes. AM J PHYSIOL-RENAL, 296(4), 859-866. [4]. http://www.ncbi.nlm.nih.gov/pubmed/19158347?dopt=Citation

Vancouver

Ackermann TF, Boini KM, Völkl H, Bhandaru M, Bareiss PM, Just L et al. SGK1-sensitive renal tubular glucose reabsorption in diabetes. AM J PHYSIOL-RENAL. 2009;296(4):859-866. 4.

Bibtex

@article{c43e3b3694e145cba578c7c66c48c55f,
title = "SGK1-sensitive renal tubular glucose reabsorption in diabetes.",
abstract = "The hyperglycemia of diabetes mellitus increases the filtered glucose load beyond the maximal tubular transport rate and thus leads to glucosuria. Sustained hyperglycemia, however, may gradually increase the maximal renal tubular transport rate and thereby blunt the increase of urinary glucose excretion. The mechanisms accounting for the increase of renal tubular glucose transport have remained ill-defined. A candidate is the serum- and glucocorticoid-inducible kinase SGK1. The kinase has been shown to stimulate Na(+)-coupled glucose transport in vitro and mediate the stimulation of electrogenic intestinal glucose transport by glucocorticoids in vivo. SGK1 expression is confined to glomerula and distal nephron in intact kidneys but may extend to the proximal tubule in diabetic nephropathy. To explore whether SGK1 modifies glucose transport in diabetic kidneys, Akita mice (akita(+/-)), which develop spontaneous diabetes, have been crossbred with gene-targeted mice lacking SGK1 on one allele (sgk1(+/-)) to eventually generate either akita(+/-)/sgk1(-/-) or akita(+/-)/sgk1(+/+) mice. Both akita(+/-)/sgk1(-/-) and akita(+/-)/sgk1(+/+) mice developed profound hyperglycemia (>20 mM) within approximately 6 wk. Body weight and plasma glucose concentrations were not significantly different between these two genotypes. However, urinary excretion of glucose and urinary excretion of fluid, Na(+), and K(+), as well as plasma aldosterone concentrations, were significantly higher in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. Studies in isolated perfused proximal tubules revealed that the electrogenic glucose transport was significantly lower in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. The data provide the first evidence that SGK1 participates in the stimulation of renal tubular glucose transport in diabetic kidneys.",
author = "Ackermann, {Teresa F} and Boini, {Krishna M} and Harald V{\"o}lkl and Madhuri Bhandaru and Bareiss, {Petra M} and Lothar Just and Volker Vallon and Kerstin Amann and Dietmar Kuhl and Yuxi Feng and Hans-Peter Hammes and Florian Lang",
year = "2009",
language = "Deutsch",
volume = "296",
pages = "859--866",
journal = "AM J PHYSIOL-RENAL",
issn = "1931-857X",
publisher = "AMER PHYSIOLOGICAL SOC",
number = "4",

}

RIS

TY - JOUR

T1 - SGK1-sensitive renal tubular glucose reabsorption in diabetes.

AU - Ackermann, Teresa F

AU - Boini, Krishna M

AU - Völkl, Harald

AU - Bhandaru, Madhuri

AU - Bareiss, Petra M

AU - Just, Lothar

AU - Vallon, Volker

AU - Amann, Kerstin

AU - Kuhl, Dietmar

AU - Feng, Yuxi

AU - Hammes, Hans-Peter

AU - Lang, Florian

PY - 2009

Y1 - 2009

N2 - The hyperglycemia of diabetes mellitus increases the filtered glucose load beyond the maximal tubular transport rate and thus leads to glucosuria. Sustained hyperglycemia, however, may gradually increase the maximal renal tubular transport rate and thereby blunt the increase of urinary glucose excretion. The mechanisms accounting for the increase of renal tubular glucose transport have remained ill-defined. A candidate is the serum- and glucocorticoid-inducible kinase SGK1. The kinase has been shown to stimulate Na(+)-coupled glucose transport in vitro and mediate the stimulation of electrogenic intestinal glucose transport by glucocorticoids in vivo. SGK1 expression is confined to glomerula and distal nephron in intact kidneys but may extend to the proximal tubule in diabetic nephropathy. To explore whether SGK1 modifies glucose transport in diabetic kidneys, Akita mice (akita(+/-)), which develop spontaneous diabetes, have been crossbred with gene-targeted mice lacking SGK1 on one allele (sgk1(+/-)) to eventually generate either akita(+/-)/sgk1(-/-) or akita(+/-)/sgk1(+/+) mice. Both akita(+/-)/sgk1(-/-) and akita(+/-)/sgk1(+/+) mice developed profound hyperglycemia (>20 mM) within approximately 6 wk. Body weight and plasma glucose concentrations were not significantly different between these two genotypes. However, urinary excretion of glucose and urinary excretion of fluid, Na(+), and K(+), as well as plasma aldosterone concentrations, were significantly higher in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. Studies in isolated perfused proximal tubules revealed that the electrogenic glucose transport was significantly lower in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. The data provide the first evidence that SGK1 participates in the stimulation of renal tubular glucose transport in diabetic kidneys.

AB - The hyperglycemia of diabetes mellitus increases the filtered glucose load beyond the maximal tubular transport rate and thus leads to glucosuria. Sustained hyperglycemia, however, may gradually increase the maximal renal tubular transport rate and thereby blunt the increase of urinary glucose excretion. The mechanisms accounting for the increase of renal tubular glucose transport have remained ill-defined. A candidate is the serum- and glucocorticoid-inducible kinase SGK1. The kinase has been shown to stimulate Na(+)-coupled glucose transport in vitro and mediate the stimulation of electrogenic intestinal glucose transport by glucocorticoids in vivo. SGK1 expression is confined to glomerula and distal nephron in intact kidneys but may extend to the proximal tubule in diabetic nephropathy. To explore whether SGK1 modifies glucose transport in diabetic kidneys, Akita mice (akita(+/-)), which develop spontaneous diabetes, have been crossbred with gene-targeted mice lacking SGK1 on one allele (sgk1(+/-)) to eventually generate either akita(+/-)/sgk1(-/-) or akita(+/-)/sgk1(+/+) mice. Both akita(+/-)/sgk1(-/-) and akita(+/-)/sgk1(+/+) mice developed profound hyperglycemia (>20 mM) within approximately 6 wk. Body weight and plasma glucose concentrations were not significantly different between these two genotypes. However, urinary excretion of glucose and urinary excretion of fluid, Na(+), and K(+), as well as plasma aldosterone concentrations, were significantly higher in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. Studies in isolated perfused proximal tubules revealed that the electrogenic glucose transport was significantly lower in akita(+/-)/sgk1(-/-) than in akita(+/-)/sgk1(+/+) mice. The data provide the first evidence that SGK1 participates in the stimulation of renal tubular glucose transport in diabetic kidneys.

M3 - SCORING: Zeitschriftenaufsatz

VL - 296

SP - 859

EP - 866

JO - AM J PHYSIOL-RENAL

JF - AM J PHYSIOL-RENAL

SN - 1931-857X

IS - 4

M1 - 4

ER -