During pregnancy, the mother must adapt her body systems to support nutrient and oxygen supply for growth of the baby in utero and during the subsequent lactation. These include changes in the cardiovascular, pulmonary, immune and metabolic systems of the mother. Failure to appropriately adjust maternal physiology to the pregnant state may result in pregnancy complications, including gestational diabetes and abnormal birth weight, which can further lead to a range of medically significant complications for the mother and baby. The placenta, which forms the functional interface separating the maternal and fetal circulations, is important for mediating adaptations in maternal physiology. It secretes a plethora of hormones into the maternal circulation which modulate her physiology and transfers the oxygen and nutrients available to the fetus for growth. Among these placental hormones, the prolactin-growth hormone family, steroids and neuropeptides play critical roles in driving maternal physiological adaptations during pregnancy. This review examines the changes that occur in maternal physiology in response to pregnancy and the significance of placental hormone production in mediating such changes.

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The Role of Placental Hormones in Mediating Maternal Adaptations to Support Pregnancy and Lactation

https://www.cell.com/current-biology/pdf/S0960-9822(10)01365-5.pdf

A molecular switch for photoperiod responsiveness in mammals.

Living organisms show seasonality in a wide array of functions such as reproduction, fattening, hibernation, and migration At temperate latitudes, changes in photoperiod maintain the alignment of annual rhythms with predictable changes in the environment The appropriate physiological response to changing photoperiod in mammals requires retinal detection of light and pineal secretion of melatonin, but extraretinal detection of light occurs in birds A common mechanism across all vertebrates is that these photoperiod-regulated systems alter hypothalamic thyroid hormone (TH) conversion Here, we review the evidence that a circadian clock within the pars tuberalis of the adenohypophysis links photoperiod decoding to local changes of TH signaling within the medio-basal hypothalamus (MBH) through a conserved thyrotropin/deiodinase axis We also focus on recent findings which indicate that, beyond the photoperiodic control of its conversion, TH might also be involved in longer-term timing processes of seasonal programs Finally, we examine the potential implication of kisspeptin and RFRP3, two RF-amide peptides expressed within the MBH, in seasonal rhythmicity

https://hal.archives-ouvertes.fr/hal-01129817/document

Thyroid hormone and seasonal rhythmicity.

In seasonally breeding vertebrates, changes in day length induce categorically distinct behavioral and reproductive phenotypes via thyroid hormone-dependent mechanisms. Winter photoperiods inhibit reproductive neuroendocrine function but cannot sustain this inhibition beyond 6 mo, ensuring vernal reproductive recrudescence. This genomic plasticity suggests a role for epigenetics in the establishment of seasonal reproductive phenotypes. Here, we report that DNA methylation of the proximal promoter for the type III deiodinase (dio3) gene in the hamster hypothalamus is reversible and critical for photoperiodic time measurement. Short photoperiods and winter-like melatonin inhibited hypothalamic DNA methyltransferase expression and reduced dio3 promoter DNA methylation, which up-regulated dio3 expression and induced gonadal regression. Hypermethylation attenuated reproductive responses to short photoperiods. Vernal refractoriness to short photoperiods reestablished summer-like methylation of the dio3 promoter, dio3 expression, and reproductive competence, revealing a dynamic and reversible mechanism of DNA methylation in the mammalian brain that plays a central role in physiological orientation in time.

https://www.pnas.org/content/pnas/110/41/16651.full.pdf

Reversible DNA methylation regulates seasonal photoperiodic time measurement

Most mammals use photoperiod to synchronize their breeding season, so that young are raised during the spring and summer months. The pineal hormone melatonin is the major endocrine message used to relay photoperiodic information to the reproductive axis. This chapter first discusses the ecological context for seasonal breeding and the pivotal role that nocturnal melatonin secretion plays in its regulation. Melatonin acts through high affinity G protein–coupled receptors, and we discuss the emergence of the pars tuberalis of the anterior pituitary as a principal site of melatonin action. We go on to discuss recent evidence that local metabolism of thyroid hormone by tanycyte cells within the mediobasal hypothalamus is the key seasonal gateway for activation of the hypothalamic gonadotropin-releasing hormone pulse generator. Melatonin controls tanycyte function via a pathway involving a novel paracrine action of thyrotropin released by pars tuberalis cells. Downstream targets of this control pathway include RF-amide neurons implicated in hypothalamic gonadotropic signaling, suggesting an integrated model for the control of seasonal reproduction in mammals. We end by focusing on current hypotheses for mechanisms of tanycyte action and the cellular consequences of altered hypothalamic triiodothyronine metabolism.

Seasonal Regulation of Reproduction in Mammals

https://www.pure.ed.ac.uk/ws/files/8172172/Dupre_et_al_2010.pdf

Chloe Duval

Papers

Identification of Eya3 and TAC1 as long-day signals in the sheep pituitary.

PTHrP is essential for normal morphogenetic and functional development of the murine placenta.