Abstract
Prenatal leptin is key to regulating foetal growth and early metabolic programming. The presence of intact leptin in rat foetal (at late gestation) and neonatal (immediately after birth) stomach content and mucosa has been previously described, suggesting that it may act as a regulatory nutrient for the neonate rats, be internalised by the stomach, and play a physiological role early in life, which requires to be further investigated, including its origin. We aimed to study the ontogeny of the presence of leptin in the foetal stomach and key extraembryonic tissues in rats at late gestation (days 18–21). Leptin concentration was determined by enzyme-linked immunosorbent assay, and placental leptin immunolocalisation was analysed by immunohistochemistry. Leptin showed a sudden appearance in the amniotic fluid (AF) at day 20 of gestation, gastric content (swallowed AF), stomach, and umbilical cord, significantly increasing at day 21. Leptin levels in these fluids and tissues were positively correlated. In the placenta, leptin was detectable at all the studied days, but its localisation changed from widespread throughout the placenta at day 18 to well-defined in the labyrinth zone from day 19 onwards. The results support a possible internalisation of AF leptin by the immature stomach of near-term foetuses and suggest that changes in placental leptin localisation might help to explain the sudden appearance of leptin in AF at gestational day 20, with potential physiological significance regarding short-term feeding control and metabolic programming in the developing offspring.
Highlights
Gestation is a high-nutritional-demand process in which optimal macro- and micronutrient supply is pivotal for foetal development, as well as for extraembryonic tissue formation and maternal tissue expansion to support foetal growth [1]
Placental weight increased with the gestational days, the increase was not continued in placentas of 21 days of gestation
Coming back to amniotic fluid leptin (AFL), despite these interspecies differences regarding AFL level progression, it is interesting to point out that leptin present in the amniotic fluid (AF) might be important for correct foetal growth and development in both species, and we speculate that the rise in AFL by mid-gestation in humans and by late gestation in rats might have a specific role
Summary
Gestation is a high-nutritional-demand process in which optimal macro- and micronutrient supply is pivotal for foetal development, as well as for extraembryonic tissue formation and maternal tissue expansion to support foetal growth [1]. Leptin has been described to play an important role in the regulation of many processes during pregnancy. Leptin from different sources, including the placenta and maternal circulation, participates in the modulation of the embryo implantation and innate and adaptive immunity, in the stimulation of nutrient uptake and protein synthesis to promote foetal growth, and in the mediation of the development of several foetal tissues [2,3,4]. It has been reported that deregulation of leptin production or availability during pregnancy could alter foetal growth through inappropriate placental development and function and program offspring to a higher risk of Nutrients 2020, 12, 2542; doi:10.3390/nu12092542 www.mdpi.com/journal/nutrients. The placenta is an important source of leptin, produced mainly by the syncytiotrophoblast cells of the labyrinth zone, and placental leptin contributes to maternal and foetal physiology, but it regulates placental development, structure, and functions. The presence of leptin receptors within the placental tissue, especially located in the syncytiotrophoblast cells as well, indicates that placental leptin exerts autocrine and paracrine functions [8,9,10,11]
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