title: [Ontogenesis of hypothalamic control of adenohypophyseal secretions in the human foetus (author's transl)].
abstract: The endocrine glands of the human foetus are active early in gestation, and various foetal and placental hormonal contributions are essential for growth and sexual differentiation. 1. The anterior pituitary gland has the ability to synthesize, store and secrete hormones early in gestation. The patterns of change in plasma concentrations of hGH (Fig. 1), ACTH, LH and FSH (Fig. 2) during gestation indicate that secretion is at a maximum at mid-gestation, followed by a progressive decrease towards term. The high levels at mid-gestation can be interpreted as due simultaneously to a high secretion rate, low peripheral catabolism and absence of feedback mechanism. In contrast, the secretions of PRL (Fig. 1) and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. 2. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence in the foetal hypothalamus of releasing factors such as LRF (Fig. 5) and TRF, and of somatostatin (Fig. 6), a growth hormone release inhibiting factor (GIF), has been established. TRF and GIF, but not LRF, are also present in the cerebral cortex. It has been postulated that, early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs, and that, later in development, there is a maturation of inhibitory or restraining influences mediated via the CNS (feedback mechanisms) that modulates the secretion of the foetal adenohypophyseal hormones (Fig. 3 and 4). 3. Observations made with anencephalic newborn confirm that a functional hypothalamus is necessary during foetal life for the secretion of each of the hormones of the anterior pituitary gland with the exception of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during foetal life, it appears evident from the anencephaly data that this regulation can only be fully understood by postulating the existence of a growth hormone releasing factor (GRF).
mesh_terms: D000757:Anencephaly / Q000097:blood; D002540:Cerebral Cortex / Q000032:analysis; D005260:Female; D005333:Fetus / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000032:analysis / Q000502:physiology; D006801:Humans; D007031:Hypothalamus / Q000032:analysis / Q000196:embryology* / Q000502:physiology; D010903:Pituitary Gland, Anterior / Q000196:embryology* / Q000378:metabolism; D010908:Pituitary Hormones, Anterior / Q000096:biosynthesis / Q000378:metabolism; D011247:Pregnancy; D013004:Somatostatin / Q000032:analysis / Q000502:physiology; D013973:Thyrotropin-Releasing Hormone / Q000032:analysis / Q000502:physiology
chemical_list: D010908:Pituitary Hormones, Anterior; D007987:Gonadotropin-Releasing Hormone; D013004:Somatostatin; D013973:Thyrotropin-Releasing Hormone
vernacular_title: Ontogenèse des fonctions hypothalamiques chez le foetus humain.