Maternal dexamethasone administration and the maturation of perirenal adipose tissue of the neonatal sheep.
Maternal dexamethasone administration promotes fetal maturation such that thermoregulation is improved following premature delivery and is thus comparable with a full term birth. In the present study we determined the impact of dexamethasone on both the mothers' metabolic status together with adipose tissue function in the newborn. Glucocorticoid action, adipokine gene expression and mitochondrial protein abundance were measured in perirenal adipose tissue of neonatal sheep that were born into either a warm (30 degrees C) or cool (15 degrees C) ambient temperature at 140 days of gestation (dGA; term approximately 147 dGA), either two days after maternal dexamethasone administration, or at 146 dGA for controls. Dexamethasone administration resulted in a reduction in maternal food intake in conjunction with raised plasma cortisol and free triiodothyronine. In offspring of dexamethasone administered mothers, plasma cortisol was lower and non-esterified fatty acids (NEFA) higher than controls. Glucocorticoid receptor (GR), 11beta-hydroxysteroid dehydrogenase (11beta-HSD1), interleukin-6 and uncoupling protein (UCP)1 and 2 mRNA together with voltage dependent anion channel, cytochrome c protein and UCP1 abundance were all increased by dexamethasone administration and being born into a cool ambient temperature. Gene expression of tumor necrosis factor alpha, adiponectin and peroxisome proliferator-activated receptor transcription factor gamma were unaffected by dexamethasone. The abundance of mRNA for the GR, 11beta-HSD1, UCP1 and 2 mRNA together with each protein were positively correlated to plasma NEFA and negatively correlated to plasma cortisol. In conclusion, despite reduced maternal food intake dexamethasone promotes maturation of glucocorticoid action and mitochondrial protein abundance in the newborn, an adaptation dependent on delivery temperature.
Gnanalingham
Mg
M
Centre for Reproduction and Early Life; Institute of Clinical Research; University of Nottingham; Nottingham UK.
Hyatt
Ma
M
Bispham
J
J
Mostyn
A
A
Clarke
L
L
Budge
H
H
Symonds
Me
M
Stephenson
T
T