The IGF's (insulin-like growth factors) are mitogenic, stimulating the fetal metabolism and coordinating the feto-placental metabolism. IGF-II regulates early embryonic development while IGF-I is responsible for the growth of the newborn (4, 5).
Fetal insulin plays an indirect role in the regulation of fetal growth. It modulates the expression of the fetal IGF. On the other hand, it has direct effects on the adipose tissue and the proliferation of the cells within the fetus. Its effects, though, on the differentiation of the tissue and thus on prenatal maturation are small.
Fetal glucocorticoid affects tissue differentiation and prenatal development of the organs such as, for example, lungs (maturation of the surfactant), liver (control of glycemia), as well as the intestines (maturation of the expression of digestive enzymes and proliferation of the villi) (6).
In addition glucocorticoid, together with thyroid gland hormones, affects the maturation of the lungs and the nervous system (18, 19).
The fetal growth hormone GH has no effects on prenatal growth. This explains the absence of growth deficiencies in congenital hypopituitarism.
Further growth factors exist that affect the proliferation, differentiation and maturation of the cells. They play an important role in embryogenesis (7, 8, 9).
- EGF (epidermal growth factors) are strongly mitogenic and form a group of molecules that bind to the same receptors (tyrosine kinase).
- TGF (transforming growth factors) form a super-family that numbers more than 30 members (TGFb, activin, BMP [bone morphogenetic proteins], compare with GDNF [glial- derived neurotropic factor]).
- FGF (fibroblast growth factors) of which around 20 are known.
Embryonic cholinesterase (ChE) is an enzyme that is active in morphogenesis. Depending on their developmental stage embryonic cells express muscarinic receptors on their surfaces for acetylcholine and synthesize cholinesterase, which is able to inactivate neurotransmitters.
The interleukins 1 form a family that belongs to the cytokines. They play an important role during implantation.
Sexual hormones with embryonic origin. Sexual differentiation occurs between the 3rd and 12th week. Responsible are genetic and also hormonal factors.
Since 1950 it is known that the secondary sexual differentiation (phenotypical gender) in contrast to primary sexual differentiation (gonadal gender) mainly depends on hormonal factors. After the 6th week Leydig's cells in the embryonic testes secrete testosterone, which is responsible for male differentiation and so leads to the genesis of the male sexual apparatus. At around the 7th week the anti-Müllerian hormone (AMH), which belongs to the TGF-b family and is secreted by Sertoli's cells, induces the atrophy of the paramesonephric ducts (Müller).
The female sexual apparatus develops spontaneously (10) when the hormonal influence mentioned above is absent. (10)