Hormones, Intrauterine Health and Programming by Jonathan R Seckl, Yves Christen

By Jonathan R Seckl, Yves Christen

The authors deal with particularly the function of hormones and their hyperlinks with different maternal environmental mediators in developmental programming. The the most important nature of the placenta as an interface and goal among maternal and foetal environments is addressed. Emphasis is made at the rising technology of epigenetics as a possible cause of how environmental occasions that take place in the course of short home windows of improvement may perhaps exert results that influence upon somatic cells via many rounds of mitosis for a lot of the lifestyles span of the following organism.

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J Clin Endocrinol Metab 87:1660–1668 Newnham JP, Jobe AH (2009) Should we be prescribing repeated courses of antenatal corticosteroids? Semin Fetal Neonatal Med 14:157–163 Nyirenda MJ, Lindsay RS, Nyirenda MJ, Lindsay RS, Kenyon CJ, Burchell A, Seckl JR (1998) Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring. J Clin Invest 101:2174–2181 O’Regan D, Kenyon CJ, Seckl JR, Holmes MC (2004) Glucocorticoid exposure in late gestation in the rat permanently programs gender-specific differences in adult cardiovascular and metabolic physiology.

2005). Prenatal exposure to synthetic glucocorticoids may also impact on the developing HPA axis: children born at term to mothers who had received glucocorticoid treatment antenatally for threatened preterm labor have higher cortisol responses to a painful stimulus on the first day of life (Davis et al. 2011) and increased responses to acute psychosocial stress in childhood (Alexander et al. 2012). The administration of low dose dexamethasone during the first trimester has also been advocated in the management of women at risk of bearing fetuses with congenital adrenal hyperplasia (CAH), and it is effective in reducing virilization in affected girls.

In terms of glucose-insulin homeostasis, although one long-term follow-up study of individuals exposed to antenatal betamethasone did not find a significant change in lipid profile or in the prevalence of diabetes or cardiovascular disease at age 30, individuals had higher insulin levels, suggesting that the risk for diabetes could increase with aging (Dalziel et al. 2005). Prenatal exposure to synthetic glucocorticoids may also impact on the developing HPA axis: children born at term to mothers who had received glucocorticoid treatment antenatally for threatened preterm labor have higher cortisol responses to a painful stimulus on the first day of life (Davis et al.

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