Endocrine glands have no ducts, are vascular, and commonly have intracellular vacuoles or granules that store their hormones.

[6] Some examples of tropic hormones secreted by the anterior pituitary gland include TSH, ACTH, GH, LH, and FSH.

At the end of the eighth week, the adrenal glands have been encapsulated and have formed a distinct organ above the developing kidneys.

One part is from the thickening of the pharyngeal floor, which serves as the precursor of the thyroxine (T4) producing follicular cells.

The other part is from the caudal extensions of the fourth pharyngobranchial pouches which results in the parafollicular calcitonin-secreting cells.

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.

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.

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.

Maternal hyperglycemia is also linked to increased insulin levels and beta cell hyperplasia in the post-term infant.

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.

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.

This stage is regulated by the secretion of insulin-like 3 (INSL3), a relaxin-like factor produced by the testicles, and the INSL3 G-coupled receptor, LGR8.

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.

An assortment of genes and proteins - such as WNT4, RSPO1, FOXL2, and various estrogen receptors - 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 and upon full development, it gives rise to the anterior pituitary gland.

The coordination of the dorsal gradient of pituitary morphogenesis is dependent on neuroectodermal signals from the infundibular bone morphogenetic protein 4 (BMP4).

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.

Hormones have diverse chemical structures, mainly of 3 classes: eicosanoids, steroids, and amino acid/protein derivatives (amines, peptides, and proteins).

[14] It occurs between adjacent cells that possess broad patches of closely opposed plasma membrane linked by transmembrane channels known as connexons.

Endocrine disease is characterized by misregulated hormone release (a productive pituitary adenoma), inappropriate response to signaling (hypothyroidism), lack of a gland (diabetes mellitus type 1, diminished erythropoiesis in chronic kidney failure), or structural enlargement in a critical site such as the thyroid (toxic multinodular goitre).

Hypofunction of endocrine glands can occur as a result of loss of reserve, hyposecretion, agenesis, atrophy, or active destruction.

Hyperfunction can occur as a result of hypersecretion, loss of suppression, hyperplastic or neoplastic change, or hyperstimulation.

[18] As the thyroid, and hormones have been implicated in signaling distant tissues to proliferate, for example, the estrogen receptor has been shown to be involved in certain breast cancers.

Dysfunction in the adrenal gland could be due to primary or secondary factors and can result in hypercortisolism or hypocortisolism.

Cushing's disease is characterized by the hypersecretion of the adrenocorticotropic hormone (ACTH) due to a pituitary adenoma that ultimately causes endogenous hypercortisolism by stimulating the adrenal glands.

[21] Graves' disease effects range from excess sweating, fatigue, heat intolerance and high blood pressure to swelling of the eyes that causes redness, puffiness and in rare cases reduced or double vision.