The Endocrinology of Human Pregnancy and Fetoplacental Neuroendocrine Development

Mesiano, Sam

doi:10.1016/b978-1-4160-4907-4.00011-5

Cited by 18 publications

(23 citation statements)

References 343 publications

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“…This sexual dimorphism in androgen production by the human fetus disappears by birth 28,42 . At midgestation, human fetal ovaries also have several steroidogenic enzymes; genes encoding multiple steroid signaling pathways; and receptors to steroids, insulin, insulin-like growth factor (IGF)-I and IGF-II 27,29,34,35 .…”

Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

“…By midgestation, the human fetal ovary has the capacity to produce and detect sex steroids, including androgen and estrogen 27,29,34–38 , with estrogen believed to regulate folliculogenesis and oocyte development in utero 39–41 . Together, endocrine (i.e., gonadotropins) and paracrine facilitators of follicular growth (i.e., androgens, growth factors such as activin and insulin-like growth factors) interact with survival and atresia factors to establish the maximal germ cell endowment of the fetal ovary, which then diminishes to about 1–2 million at birth and 300,000 by menarche 28,32 .…”

Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

“…During the second trimester of human fetal development, a transient rise of pituitary gonadotropins increases androgen production by the testes compared to the ovary, temporarily elevating circulating androgen levels in the male compared to the female fetus 28,42 . This sexual dimorphism in androgen production by the human fetus disappears by birth 28,42 .…”

Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

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Intrauterine Environment and Polycystic Ovary Syndrome

et al. 2014

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The maternal-fetal environment plays an important role in developmental programming of adult disease. Metabolic and hormonal dysfunction during human fetal development accompanies gestational diabetes as a common occurrence in polycystic ovary syndrome (PCOS) mothers, while human fetal androgen excess from congenital adrenal hyperplasia or virilizing tumors precedes PCOS-like symptoms after birth. To date, clinical studies of infant blood levels at term have yet to confirm that human fetal androgen excess promotes PCOS development after birth. Earlier in development, however, circulating androgen levels in the second trimester female human fetus can normally rise into the male range. Furthermore, midgestational amniotic testosterone levels are elevated in female fetuses of PCOS compared to normal mothers and might influence fetal development, since experimentally-induced fetal androgen excess in animals produces a PCOS-like phenotype with reproductive and metabolic dysfunction. Such alterations in the maternal-fetal environment likely program adult PCOS by epigenetic modifications of genetic susceptibility of the fetus to PCOS after birth. Understanding this phenomenon requires advanced fetal surveillance technologies and postnatal assessment of midgestational androgen exposure for new clinical strategies to improve reproduction in PCOS women, optimize long-term health of their offspring, and minimize susceptibility to acquiring PCOS in future generations.

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Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

Section: Ontogeny Of the Human Fetal Ovarymentioning

confidence: 99%

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Intrauterine Environment and Polycystic Ovary Syndrome

et al. 2014

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“…Normal FSHr are very weakly stimulated during pregnancy, because FSH is almost undetectable in the serum (15). The mutations are thought to induce a structural change in the FSHr, causing an increase in constitutive activity and a decrease in the specificity barrier toward hCG.…”

mentioning

confidence: 99%

Does elevated human chorionic gonadotropin alone trigger spontaneous ovarian hyperstimulation syndrome?

Michaelson‐Cohen

Altarescu

Beller

et al. 2008

Fertility and Sterility

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“…In humans, an endocrine feedback mechanism prepares the endometrium for implantation and placentation [5] and mother-embryo interactions that lead to the formation of the placenta are a first crucial step to secure a pregnancy's chance of successful progression. While all primates establish an early connection between the maternal blood supply and the embryo, there is a major difference in embryo implantation and pregnancy progression among primates.…”

Section: Introductionmentioning

confidence: 99%

Adaptive evolution at immune system genes and deep pregnancy implantation in primates

Civetta

2015

Genomics

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A major evolutionary change in the lineage ancestral to humans, chimpanzee and gorilla (HCG) has been the embedding of the embryo into maternal tissue. Thus, the first layer of cells (trophoblast) to differentiate after fertilization must adapt to invade the uterus. Such event would likely leave signatures of positive selection at genes with roles in embryo implantation. Here, 163 pregnancy implantation genes are tested for evidence of adaptive diversification in the ancestral lineage to HCG. Two immune system genes, HLA-E and KIR2DL4 showed evidence of positive selection. Some of the positive selected sites involve amino acid substitution with predicted damaging effects on protein function, thus highlighting the possibility of antagonistic pleiotropic effects. Selection at a gene coding for a receptor expressed in uterine cells (KIR) that interacts with trophoblast human leukocyte antigen (HLA) genes suggests a main role for immunological adaptations in embryo deep invasion of the maternal endometrium.

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The Endocrinology of Human Pregnancy and Fetoplacental Neuroendocrine Development

Cited by 18 publications

References 343 publications

Intrauterine Environment and Polycystic Ovary Syndrome

Intrauterine Environment and Polycystic Ovary Syndrome

Does elevated human chorionic gonadotropin alone trigger spontaneous ovarian hyperstimulation syndrome?

Adaptive evolution at immune system genes and deep pregnancy implantation in primates

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