[Prenatal exposure to androgens as a factor of fetal programming].
Both epidemiological and clinical evidence suggest a relationship between the prenatal environment and the risk of developing diseases during adulthood. The first observations about this relationship showed that prenatal growth retardation or stress conditions during fetal life were associated to cardiovascular, metabolic and other diseases in later life. However, not only those conditions may have lasting effects after birth. Growing evidence suggests that prenatal exposure to steroids (either of fetal or maternal origin) could be another source of prenatal programming with detrimental consequences during adulthood. We have recently demonstrated that pregnant women with polycystic ovary syndrome exhibit elevated androgen levels compared to normal pregnant women, which could provide an androgen excess for both female or male fetuses. We have further tested this hypothesis in an animal model of prenatal androgenization, finding that females born from androgenized mothers have a low birth weight and high insulin resistance, that starts at an early age. On the other hand, males have low testosterone and LH secretion in response to a GnRH analogue test compared to control males and alterations in seminal parameters. We therefore propose that our efforts should be directed to modify the hyperandrogenic intrauterine environment to reduce the potential development of reproductive and metabolic diseases during adulthood.
Laboratorio de Fisiología y Endocrinología Animal, Facultad de Medicina Veterinaria, Departamento de Ciencias Animales, Universidad de Concepción, Chillán.
Sergio E
SE
Recabarren
Teresa
T
Sir-Petermann
Manuel
M
Maliqueo
Alejandro
A
Lobos
Pedro
P
Rojas-García
D000728:Androgens / Q000378:metabolism*; D000818:Animals; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications* / Q000378:metabolism; D008297:Male; D011085:Polycystic Ovary Syndrome / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D000728:Androgens