
The Library
Role of maternal glucocorticoid inducible kinase SGK1 in fetal programming of blood pressure in response to prenatal diet
Tools
Rexhepaj, R., Boini, K. M., Huang, D. Y., Amann, K., Artunc, F., Wang, K., Brosens, Jan J., Kuhl, D. and Lang, F. (2008) Role of maternal glucocorticoid inducible kinase SGK1 in fetal programming of blood pressure in response to prenatal diet. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Vol.294 (No.6). R2008-R2013. doi:10.1152/ajpregu.00737.2007 ISSN 0363-6119.
Research output not available from this repository.
Request-a-Copy directly from author or use local Library Get it For Me service.
Official URL: http://dx.doi.org/10.1152/ajpregu.00737.2007
Abstract
Maternal stress and malnutrition modify intrauterine fetal development with impact on postnatal blood pressure, nutrient, water, and electrolyte metabolism. The present study explored the possible involvement of maternal serum- and glucocorticoid-inducible kinase (SGK)-1 in fetal programming of blood pressure. To this end, wild-type (sgk1+/+) male mice were mated with SGK1 knockout (sgk1−/−) female mice, and sgk1−/− males with sgk1+/+ females, resulting in both cases in heterozygotic (sgk1−/+) offspring. Following prenatal protein restriction, the offspring of sgk1+/+ mothers gained weight significantly slower and had significantly higher blood pressure after birth. Moreover, a sexual dimorphism was apparent in fasting blood glucose and plasma corticosterone concentrations, with higher levels in female offspring. In contrast, prenatal protein restriction of sgk1−/− mothers had no significant effect on postnatal weight gain, blood pressure, plasma glucose concentration, or corticosterone levels, irrespective of offspring sex. Plasma aldosterone concentration, urinary flow rates, and urinary excretions of Na+ and K+ were not significantly modified by either maternal genotype or nutritional manipulation. In conclusion, maternal signals mediated by SGK1 may play a decisive role in fetal programming of hypertension induced by prenatal protein restriction.
Item Type: | Journal Article | ||||
---|---|---|---|---|---|
Subjects: | R Medicine > R Medicine (General) | ||||
Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Reproductive Health ( - until July 2016) Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
||||
Journal or Publication Title: | American Journal of Physiology: Regulatory, Integrative and Comparative Physiology | ||||
Publisher: | American Physiological Society | ||||
ISSN: | 0363-6119 | ||||
Official Date: | June 2008 | ||||
Dates: |
|
||||
Volume: | Vol.294 | ||||
Number: | No.6 | ||||
Page Range: | R2008-R2013 | ||||
DOI: | 10.1152/ajpregu.00737.2007 | ||||
Status: | Peer Reviewed | ||||
Publication Status: | Published | ||||
Access rights to Published version: | Restricted or Subscription Access |
Request changes or add full text files to a record
Repository staff actions (login required)
![]() |
View Item |