Mechanisms of lipid metabolism in uterine receptivity and embryo development

The quality of embryo implantation, depending on uterine receptivity and early embryo development during early pregnancy, determines ongoing pregnancy efficiency. Lipid metabolism, including phospholipid, sphingolipid, and cholesterol metabolism, regulates embryo development, implantation, and uterine decidualization. Maternal lipid metabolism signaling regulates the reproductive axis through hypothalamic neurons. Lipid metabolism and fatty acids regulate early embryo development potential and modulate embryonic epigenetic modification. Metabolic regulation plays important roles in embryo development and uterine receptivity during early pregnancy, ultimately influencing pregnancy efficiency in mammals. The important roles of lipid metabolism during early pregnancy have not been fully understood. Here, we described the regulatory roles of phospholipid, sphingolipid, and cholesterol metabolism on early embryo development, implantation, and uterine receptivity through production of cannabinoids, prostaglandins, lysophosphatidic acid, sphingosine-1-phosphate, and steroid hormones. Moreover, the impacts of lipids and fatty acids on embryo development potential and the related epigenetic modifications are also discussed. This review aims to elucidate the modulations of lipid metabolism on uterine receptivity and embryo development, contributing to novel strategies to establish dietary balanced lipids and fatty acids for reducing early embryo loss. Metabolic regulation plays important roles in embryo development and uterine receptivity during early pregnancy, ultimately influencing pregnancy efficiency in mammals. The important roles of lipid metabolism during early pregnancy have not been fully understood. Here, we described the regulatory roles of phospholipid, sphingolipid, and cholesterol metabolism on early embryo development, implantation, and uterine receptivity through production of cannabinoids, prostaglandins, lysophosphatidic acid, sphingosine-1-phosphate, and steroid hormones. Moreover, the impacts of lipids and fatty acids on embryo development potential and the related epigenetic modifications are also discussed. This review aims to elucidate the modulations of lipid metabolism on uterine receptivity and embryo development, contributing to novel strategies to establish dietary balanced lipids and fatty acids for reducing early embryo loss. in early embryo development, both the paternal and maternal genomes must undergo chromatin demethylation and zygote genomic methylation to initially establish the gene expression patterns for embryo development. a dynamic developmental process that involves a series of physiological and biochemical reactions between the trophoblast cells of blastocysts and the luminal epithelium, glandular epithelium, and stromal cells of the uterus. There are three stages to implantation: localization, adhesion, and invasion. When the uterine cavity fluid is absorbed and causes closure of the uterine cavity, the embryonic trophoblastic layer approaches the endometrial epithelium, then the embryos adhere to the luminal epithelium, thereby invading into the uterine stromal cell layer, accompanied by increased permeability of endometrial vessels. ovarian steroidogenesis is manipulated by the hypothalamic–pituitary–gonadal axis (reproductive axis), which is mainly modulated by hypothalamic gonadotropin-releasing hormone (GnRH) neurons synthesizing and releasing GnRH in a pulsed manner into the pituitary gland to generate luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and as a result of that, LH and FSH send signals to the gonad and trigger progesterone and estrogen production in the ovaries. a series of morphological changes of the uterus in early pregnancy in humans, which is essential for subsequent placenta formation and fetal development. The decidualization signal is generated through two types of cell–cell interactions, namely, embryo–endometrial epithelium interactions and endometrial epithelium–matrix interactions.