Lack of effect of nicotine or ethanol on the activity of 11β- hydroxysteroid dehydrogenase type 2

Rafn Benediktsson; Ebba M. Magnusdottir; Jonathan R. Seckl

doi:10.1016/S0960-0760(97)00086-1

Lack of effect of nicotine or ethanol on the activity of 11β- hydroxysteroid dehydrogenase type 2

Rafn Benediktsson
, Ebba M. Magnusdottir
, Jonathan R. Seckl

Háskóli Íslands, Landspítali

Rannsóknarafurð: Framlag til fræðitímarits › Grein › ritrýni

Útdráttur

Low birth weight in combination with a large placenta predicts human hypertension. The pathophysiological link remains unclear, but glucocorticoid excess impairs fetal growth and leads to offspring hypertension. A key controller of fetal glucocorticoid exposure and local tissue availability is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). The activity of placental 11β-HSD2 correlates with fetal growth in animals and humans. Ethanol abuse and smoking are known to retard fetal growth which may relate to altered glucocorticoid action or dynamics. This study has examined whether nicotine or ethanol modulate glucocorticoid action in the placenta or fetus by inhibiting 11β-HSD2, using clonal cell cultures, freshly isolated dually perfused intact human placentas and placentas from in vivo treated rats. No significant effect on the activity of 11β-HSD2 by pathophysiologically relevant nicotine or ethanol concentrations was observed. The mechanism of action of nicotine and ethanol relevant to reduced fetal growth requires further study.

Upprunalegt tungumál	Enska
Síður (frá-til)	303-307
Síðufjöldi	5
Fræðitímarit	Journal of Steroid Biochemistry and Molecular Biology
Bindi	63
Númer tölublaðs	4-6
DOI	https://doi.org/10.1016/S0960-0760(97)00086-1
Útgáfustaða	Útgefið - nóv. 1997

Athugasemd

Funding Information: Acknowledgements--This work has been supported by a Wellcome Trust Advanced Training Fellowship (RB) a Wellcome Senior Clinical Fellowship ORS) and grants from the Wellcome Trust, the Scottish Hospital Endowments Research Trust, the Medical Research Council and the Sir Stanley and Lady Davidson Medical Research Fund. We would like to thank Mrs. Jill C. Smith for technical assistance, staff at the Simpson Memorial Maternity Pavilion in Edinburgh for help with help with collecting placentas and Dr. Caroline Leckie for providing LLC-PK1 cells.

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10.1016/S0960-0760(97)00086-1

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@article{ad65328855594ca0bff96d5964b9f9d8,

title = "Lack of effect of nicotine or ethanol on the activity of 11β- hydroxysteroid dehydrogenase type 2",

abstract = "Low birth weight in combination with a large placenta predicts human hypertension. The pathophysiological link remains unclear, but glucocorticoid excess impairs fetal growth and leads to offspring hypertension. A key controller of fetal glucocorticoid exposure and local tissue availability is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). The activity of placental 11β-HSD2 correlates with fetal growth in animals and humans. Ethanol abuse and smoking are known to retard fetal growth which may relate to altered glucocorticoid action or dynamics. This study has examined whether nicotine or ethanol modulate glucocorticoid action in the placenta or fetus by inhibiting 11β-HSD2, using clonal cell cultures, freshly isolated dually perfused intact human placentas and placentas from in vivo treated rats. No significant effect on the activity of 11β-HSD2 by pathophysiologically relevant nicotine or ethanol concentrations was observed. The mechanism of action of nicotine and ethanol relevant to reduced fetal growth requires further study.",

author = "Rafn Benediktsson and Magnusdottir, \{Ebba M.\} and Seckl, \{Jonathan R.\}",

note = "Funding Information: Acknowledgements--This work has been supported by a Wellcome Trust Advanced Training Fellowship (RB) a Wellcome Senior Clinical Fellowship ORS) and grants from the Wellcome Trust, the Scottish Hospital Endowments Research Trust, the Medical Research Council and the Sir Stanley and Lady Davidson Medical Research Fund. We would like to thank Mrs. Jill C. Smith for technical assistance, staff at the Simpson Memorial Maternity Pavilion in Edinburgh for help with help with collecting placentas and Dr. Caroline Leckie for providing LLC-PK1 cells.",

year = "1997",

month = nov,

doi = "10.1016/S0960-0760(97)00086-1",

language = "English",

volume = "63",

pages = "303--307",

journal = "Journal of Steroid Biochemistry and Molecular Biology",

issn = "0960-0760",

publisher = "Elsevier Ltd.",

number = "4-6",

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TY - JOUR

T1 - Lack of effect of nicotine or ethanol on the activity of 11β- hydroxysteroid dehydrogenase type 2

AU - Benediktsson, Rafn

AU - Magnusdottir, Ebba M.

AU - Seckl, Jonathan R.

N1 - Funding Information: Acknowledgements--This work has been supported by a Wellcome Trust Advanced Training Fellowship (RB) a Wellcome Senior Clinical Fellowship ORS) and grants from the Wellcome Trust, the Scottish Hospital Endowments Research Trust, the Medical Research Council and the Sir Stanley and Lady Davidson Medical Research Fund. We would like to thank Mrs. Jill C. Smith for technical assistance, staff at the Simpson Memorial Maternity Pavilion in Edinburgh for help with help with collecting placentas and Dr. Caroline Leckie for providing LLC-PK1 cells.

PY - 1997/11

Y1 - 1997/11

N2 - Low birth weight in combination with a large placenta predicts human hypertension. The pathophysiological link remains unclear, but glucocorticoid excess impairs fetal growth and leads to offspring hypertension. A key controller of fetal glucocorticoid exposure and local tissue availability is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). The activity of placental 11β-HSD2 correlates with fetal growth in animals and humans. Ethanol abuse and smoking are known to retard fetal growth which may relate to altered glucocorticoid action or dynamics. This study has examined whether nicotine or ethanol modulate glucocorticoid action in the placenta or fetus by inhibiting 11β-HSD2, using clonal cell cultures, freshly isolated dually perfused intact human placentas and placentas from in vivo treated rats. No significant effect on the activity of 11β-HSD2 by pathophysiologically relevant nicotine or ethanol concentrations was observed. The mechanism of action of nicotine and ethanol relevant to reduced fetal growth requires further study.

AB - Low birth weight in combination with a large placenta predicts human hypertension. The pathophysiological link remains unclear, but glucocorticoid excess impairs fetal growth and leads to offspring hypertension. A key controller of fetal glucocorticoid exposure and local tissue availability is 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). The activity of placental 11β-HSD2 correlates with fetal growth in animals and humans. Ethanol abuse and smoking are known to retard fetal growth which may relate to altered glucocorticoid action or dynamics. This study has examined whether nicotine or ethanol modulate glucocorticoid action in the placenta or fetus by inhibiting 11β-HSD2, using clonal cell cultures, freshly isolated dually perfused intact human placentas and placentas from in vivo treated rats. No significant effect on the activity of 11β-HSD2 by pathophysiologically relevant nicotine or ethanol concentrations was observed. The mechanism of action of nicotine and ethanol relevant to reduced fetal growth requires further study.

UR - https://www.scopus.com/pages/publications/0031405073

U2 - 10.1016/S0960-0760(97)00086-1

DO - 10.1016/S0960-0760(97)00086-1

M3 - Article

C2 - 9459196

SN - 0960-0760

VL - 63

SP - 303

EP - 307

JO - Journal of Steroid Biochemistry and Molecular Biology

JF - Journal of Steroid Biochemistry and Molecular Biology

IS - 4-6

ER -

Lack of effect of nicotine or ethanol on the activity of 11β- hydroxysteroid dehydrogenase type 2

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