Glucocorticoid exposure and tissue gene expression of 11β HSD-1, 11β HSD-2, and glucocorticoid receptor in a porcine model of differential fetal growth

Mar 24, 2007Reproduction (Cambridge, England)

Glucocorticoid levels and related gene activity in different fetal growth stages in pigs

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Abstract

At day 45 of gestation, small fetuses had a plasma cortisol level of 16.8 +/- 3.4 ng/ml, significantly lower than the 34.4 +/- 3.4 ng/ml observed in average-sized fetuses (P < 0.001).

By day 65, cortisol levels in small and average fetuses were similar, with concentrations of 5.7 +/- 1.0 ng/ml and 4.8 +/- 0.5 ng/ml, respectively (P = 0.128).
At day 100, small fetuses exhibited elevated cortisol levels of 10.7 +/- 1.5 ng/ml compared to 7.6 +/- 0.7 ng/ml in average fetuses (P < 0.001).
Maternal plasma cortisol levels remained stable throughout gestation, averaging around 56 ng/ml.
Alterations in cortisol supply appear to originate from the fetus rather than maternal sources.
Fetal organs showed different patterns of gene expression for cortisol metabolism, indicating varying sensitivity to cortisol, especially in the liver during late gestation.

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Glucocorticoids play a critical role in fetal development, but inappropriate exposure is associated with reduced fetal growth. We investigated cortisol exposure and supply in a porcine model of differential fetal growth. This model compares the smallest fetus of a litter with an average-sized sibling at three stages of gestation. At day 45, small fetuses had reduced plasma cortisol (16.8 +/- 3.4 ng/ml) relative to average fetuses (34.4 +/- 3.4 ng/ml, P < 0.001). At day 65 levels had reduced in small and average fetuses to similar concentrations (5.7 +/- 1.0 vs 4.8 +/- 0.5 ng/ml, P = 0.128). By day 100, elevated levels were found in small fetuses (10.7 +/- 1.5 vs 7.6 +/- 0.7 ng/ml, P < 0.001). Maternal plasma cortisol was unchanged over gestation (day 45, 56.7 +/- 21.6 ng/ml; day 65, 57.8 +/- 14.4 ng/ml; day 100, 55.7 +/- 6.5 ng/ml). We examined the cause of altered cortisol by investigating the fetal hypothalamic-pituitary-adrenal axis through the measurement of adrenocorticotropic hormone and assessing exposure to maternal cortisol by quantifying placental 11beta-hydroxysteroid dehydrogenase-isoform 2 (11beta HSD-2) gene expression. These data suggest that altered cortisol supply was of fetal origin. We examined organ glucocorticoid (GC) metabolism by the measurement of GC receptor (GR) and 11beta-hydroxysteroid dehydrogenase-isoform 1 (11beta HSD-1) gene expression. We found that fetal organs have different temporal patterns of 11beta HSD-1 and GR expression, with the liver particularly sensitive to cortisol in late gestation. This study examines GC exposure in naturally occurring differential growth and simultaneously explores tissue GC sensitivity and handling, at three key stages of gestation.

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Glucocorticoid exposure and tissue gene expression of 11β HSD-1, 11β HSD-2, and glucocorticoid receptor in a porcine model of differential fetal growth

Abstract

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