ESTIMULACION INTRAUTERINA PDF

Prenatal exposure to androgens as a factor of fetal programming. Sergio E. 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.

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Prenatal exposure to androgens as a factor of fetal programming. Sergio E. 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. Key-words : Androgens; Fetal growth retardation; Prenatal exposure delayed effects.

Por lo tanto, se considera en la actualidad, que un disruptor endocrino es cualquier hormona que produce un desbalance en el sistema endocrino Recientemente, se ha descrito que las hembras nacidas de ovejas androgenizadas tienen un menor peso al nacimiento y un crecimiento compensatorio a los meses de vida postnatal 31,32 , lo que no se ha observado en los machos nacidos de hembras androgenizadas. Lucas A. Programming by early nutrition in man. En: Block G.

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Lancet ; Ovulation in prenatal androgenized ewes. J Endocrinol ; Insights into the development of polycystic ovary syndrome PCOS from studies of prenatally androgenized female rhesus monkeys. Trends Endocrinol Metab ; 9: Ozanne SE. Metabolic programming in animals. Br Med Bull ; Effects of prenatal testosterone propionate on the sexual development of male and female rats: a dose-response study.

Toxicol Sci ; Prenatal programming of reproductive neuroendocrine function: fetal androgen exposure produces progressive disruption of reproductive cycles in sheep.

Fetal programming: prenatal exposure to excess testosterone programs hyperinsulinemia. Biol Reprod ; 68 Suppl 1 Abstract Postnatal developmental consequences of altered insulin sensitivity in female sheep treated prenatally with testosterone. Am J Physiol Endocrinol Metab ; Fetal programming: Prenatal testosterone excess leads to fetal growth retardation and postnatal catch-up growth in sheep. Prenatal dihydrotestosterone differentially masculinizes tonic and surge modes of luteinizing hormone secretion in sheep.

Fetal programming: prenatal androgen disrupts positive feedback actions of estradiol but does not affect timing of puberty in female sheep. Biol Reprod ; New MI. Factors determining final height in congenital adrenal hyperplasia. J Pediatr Endocrinol Metab ; 14 Suppl 2 : Prenatal diagnosis for congenital adrenal hyperplasia in pregnancies.

J Clin Endocrinol Metab ; Behavioral effects of prenatal versus postnatal androgen excess in children with hydroxylase-deficient congenital adrenal hyperplasia. Timing of prenatal androgen excess determines differential impairment in insulin secretion and action in adult female rhesus monkeys. Ovarian hyperandrogenism in adult female rhesus monkeys exposed to prenatal androgen excess. Fertil Steril ; Response to the gonadotropin releasing hormone agonist leuprolide in immature female sheep androgenized in utero.

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