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This Article Full Text Full Text (PDF) All Versions of this Article: 294/6/R2008    most recent 00737.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Rexhepaj, R. Articles by Lang, F. PubMed PubMed Citation Articles by Rexhepaj, R. Articles by Lang, F.

WATER AND ELECTROLYTE HOMEOSTASIS

Role of maternal glucocorticoid inducible kinase SGK1 in fetal programming of blood pressure in response to prenatal diet

Departments of ¹Physiology and ²Pharmacology, University of Tübingen, Tübingen; and ³Department of Pathology, University of Erlangen, Erlangen, Germany; ⁴Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London, United Kingdom; and ⁵Department of Biology, Chemistry, and Pharmacy, Free University, Berlin, Berlin, Germany

Submitted 10 October 2007 ; accepted in final form 19 March 2008

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.

dietary protein; body weight; plasma glucose