Jørgen Frøkiær

Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats

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Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats. / Tingskov, Stine Julie; Hu, Shan; Frøkiær, Jorgen et al.

In: American Journal of Physiology: Renal Physiology, Vol. 314, No. 5, 05.2018, p. F1020-F1025.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

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Tingskov, SJ, Hu, S, Frøkiær, J, Kwon, T-H, Wang, W & Norregaard, R 2018, 'Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats', American Journal of Physiology: Renal Physiology, vol. 314, no. 5, pp. F1020-F1025. https://doi.org/10.1152/ajprenal.00604.2017

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Tingskov, Stine Julie ; Hu, Shan ; Frøkiær, Jorgen et al. / Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats. In: American Journal of Physiology: Renal Physiology. 2018 ; Vol. 314, No. 5. pp. F1020-F1025.

Bibtex

@article{994f1c45cb4446ed9245c4bcdcff8caf,
title = "Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats",
abstract = "Lithium is widely used in treatment of bipolar affective disorders, but often causes nephrogenic diabetes insipidus (NDI), a disorder characterized by severe urinary concentrating defects. Lithium-induced NDI is caused by lithium uptake by collecting duct principal cells and altered expression of aquaporin-2 (AQP2), which are essential for water reabsorption of tubular fluid in the collecting duct. Sex hormones have previously been shown to affect the regulation of AQP2, so we tested whether tamoxifen (TAM), a selective estrogen receptor modulator, would attenuate lithium-induced alterations on renal water homeostasis. Rats were treated for 14 days with lithium and TAM treatment was initiated one week after onset of lithium administration. Lithium treatment resulted in severe polyuria and reduced AQP2 expression, which was ameliorated by TAM. Consistent with this, TAM attenuated downregulation of AQP2 and increased phosphorylation of the cAMP responsive element binding protein (CREB), which induced AQP2 expression, in freshly isolated inner medullary collecting duct suspension prepared from lithium-treated rats. In conclusion, TAM attenuated dose-dependently polyuria, impaired urine concentration, and downregulation of AQP2 protein expression in rats with lithium-induced NDI. These findings suggest that TAM is likely to be a novel therapeutic option for lithium-induced NDI.",
keywords = "Journal Article",
author = "Tingskov, {Stine Julie} and Shan Hu and Jorgen Fr{\o}ki{\ae}r and Tae-Hwan Kwon and Weidong Wang and Rikke Norregaard",
year = "2018",
month = may,
doi = "10.1152/ajprenal.00604.2017",
language = "English",
volume = "314",
pages = "F1020--F1025",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "5",

}

RIS

TY - JOUR

T1 - Tamoxifen attenuates development of lithium-induced nephrogenic diabetes insipidus in rats

AU - Tingskov, Stine Julie

AU - Hu, Shan

AU - Frøkiær, Jorgen

AU - Kwon, Tae-Hwan

AU - Wang, Weidong

AU - Norregaard, Rikke

PY - 2018/5

Y1 - 2018/5

N2 - Lithium is widely used in treatment of bipolar affective disorders, but often causes nephrogenic diabetes insipidus (NDI), a disorder characterized by severe urinary concentrating defects. Lithium-induced NDI is caused by lithium uptake by collecting duct principal cells and altered expression of aquaporin-2 (AQP2), which are essential for water reabsorption of tubular fluid in the collecting duct. Sex hormones have previously been shown to affect the regulation of AQP2, so we tested whether tamoxifen (TAM), a selective estrogen receptor modulator, would attenuate lithium-induced alterations on renal water homeostasis. Rats were treated for 14 days with lithium and TAM treatment was initiated one week after onset of lithium administration. Lithium treatment resulted in severe polyuria and reduced AQP2 expression, which was ameliorated by TAM. Consistent with this, TAM attenuated downregulation of AQP2 and increased phosphorylation of the cAMP responsive element binding protein (CREB), which induced AQP2 expression, in freshly isolated inner medullary collecting duct suspension prepared from lithium-treated rats. In conclusion, TAM attenuated dose-dependently polyuria, impaired urine concentration, and downregulation of AQP2 protein expression in rats with lithium-induced NDI. These findings suggest that TAM is likely to be a novel therapeutic option for lithium-induced NDI.

AB - Lithium is widely used in treatment of bipolar affective disorders, but often causes nephrogenic diabetes insipidus (NDI), a disorder characterized by severe urinary concentrating defects. Lithium-induced NDI is caused by lithium uptake by collecting duct principal cells and altered expression of aquaporin-2 (AQP2), which are essential for water reabsorption of tubular fluid in the collecting duct. Sex hormones have previously been shown to affect the regulation of AQP2, so we tested whether tamoxifen (TAM), a selective estrogen receptor modulator, would attenuate lithium-induced alterations on renal water homeostasis. Rats were treated for 14 days with lithium and TAM treatment was initiated one week after onset of lithium administration. Lithium treatment resulted in severe polyuria and reduced AQP2 expression, which was ameliorated by TAM. Consistent with this, TAM attenuated downregulation of AQP2 and increased phosphorylation of the cAMP responsive element binding protein (CREB), which induced AQP2 expression, in freshly isolated inner medullary collecting duct suspension prepared from lithium-treated rats. In conclusion, TAM attenuated dose-dependently polyuria, impaired urine concentration, and downregulation of AQP2 protein expression in rats with lithium-induced NDI. These findings suggest that TAM is likely to be a novel therapeutic option for lithium-induced NDI.

KW - Journal Article

U2 - 10.1152/ajprenal.00604.2017

DO - 10.1152/ajprenal.00604.2017

M3 - Journal article

C2 - 29357422

VL - 314

SP - F1020-F1025

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 5

ER -