Development of the endocrine system
In contrast, endocrine glands that arise from the endoderm and ectoderm produce the amine, peptide, and protein hormones.
At the end of the eighth week, the adrenal glands have been encapsulated and have formed a distinct organ above the developing kidneys.
Around the 24th day of pregnancy, the foramen cecum, a thin, flask-like diverticulum of the median anlage develops.
During fetal development, T4 is the major thyroid hormone being produced while triiodothyronine (T3) and its inactive derivative, reverse T3, are not detected until the third trimester.
Reaching eight to ten weeks into development, the pancreas starts producing insulin, glucagon, somatostatin, and pancreatic polypeptide.
[citation needed] While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the amount of insulin that is released into the bloodstream is relatively low.
[14] In contrast to insulin, the fetal plasma glucagon levels are relatively high and continue to increase during development.
[16] However, a study of an infusion of alanine into pregnant women was shown to increase the cord blood and maternal glucagon concentrations, demonstrating a fetal response to amino acid exposure.
On the other hand, the stable fetal serum glucose levels could be attributed to the absence of pancreatic signaling initiated by incretins during feeding.
Fetal insulin is responsible for increasing glucose uptake and lipogenesis during the stages leading up to birth.
[15] This temporary physiological change aids the increased rate of fetal development during the final trimester.
Maternal hyperglycemia is also linked to increased insulin levels and beta cell hyperplasia in the post-term infant.
[16] Children of diabetic mothers are at an increased risk for conditions such as: polycythemia, renal vein thrombosis, hypocalcemia, respiratory distress syndrome, jaundice, cardiomyopathy, congenital heart disease, and improper organ development.
Once synthesized, the anti-Müllerian hormone initiates the ipsilateral regression of the Müllerian tract and inhibits the development of female internal features.
[18] The testicles descend during prenatal development in a two-stage process that begins at eight weeks of gestation and continues through the middle of the third trimester.
During the second and third trimester, testicular development concludes with the diminution of the fetal Leydig cells and the lengthening and coiling of the seminiferous cords.
The Müllerian structures remain and develop into the fallopian tubes, uterus, and the upper region of the vagina.
[20] An assortment of genes and proteins - such as WNT4,[21] RSPO1,[22] FOXL2,[23] and various estrogen receptors[24] - have been shown to prevent the development of testicles or the lineage of male-type cells.
The Rathke's pouch, a cavity of ectodermal cells of the oropharynx, forms between the fourth and fifth week of gestation[26] and upon full development, it gives rise to the anterior pituitary gland.
[29][30] The coordination of the dorsal gradient of pituitary morphogenesis is dependent on neuroectodermal signals from the infundibular bone morphogenetic protein 4 (BMP4).
[32] Ventral developmental patterning and the expression of transcription factors is influenced by the gradients of BMP2 and sonic hedgehog protein (SHH).
Within eight weeks of gestation, somatotroph cells begin to develop with cytoplasmic expression of human growth hormone.
