Fetal Adrenal Cortex Research Articles

Excretion of steroids by the newborn infant

The entire excreta from babies during the first few days after birth were extracted and analyzed for neutral steroids related to hormonal function. Material giving the Zimmermann reaction was found in the ketonic fraction, but no reaction with the antimony trichloride reaction of Pincus was obtained. The nonketonic fraction gave the antimony trichloride reaction. Both the ketonic Zimmermann-positive and the nonketonic antimony trichloride-positive substances decreased to very low levels during the first 10 days after birth. The material responsible for the color reaction in the nonketonic fraction was identified as androstane-3α, 17β-diol, probably a metabolic product of compounds formed in the fetal adrenal cortex.

C19 steroids, 17alpha-hydroxycorticosterone and a sodium retaining factor in human fetal adrenal glands.

THE embryological development of the human fetal adrenal cortex, and, perhaps, other primates, is unique. During the second month of fetal life, a distinct adrenal cortex is recognized. It reaches its largest relative size during the third and fourth month when it occupies about 0.5% of the total body volume as compared to 0.01% in the adult (Jackson, 1909). The histological picture of the fetal adrenal cortex differs from that of the adult by the presence of the fetal zone, which comprises about 80% of the whole cortex. The fetal zone degenerates rapidly during the first post-natal months. In addition, only the glomerular and fascicular zones of the cortex are fairly well developed in the fetus (Lanman, 1953). In contrast to the available data on the morphology and anatomy of the human fetal adrenal cortex, its physiology remains largely unknown. An excellent review of the subject has been published by Lanman (1953). Large amounts of ascorbic acid (Bourne, 1933) and lipid material (Lanman, 1953) have bee...

A study of the interrelationships of maternal and fetal adrenal glands of rats.

DURING pregnancy in the human (Venning, 1946; Tobian, 1949; Devis and Devis-Vanden Eeckhoudt, 1949; Jailer and Knowlton, 1950; Lloyd et al., 1952) or in the experimental animals, (Anderson and Sperry, 1937) secretory activity of the adrenal cortex of the mother appears to be high. Little is known about the activity of the fetal adrenal cortex and the interrelationships of maternal and fetal adrenals have not been widely studied. Firor and Grollman (1933) observed that adrenalectomized pregnant albino rats survived twice as long as nonpregnant controls. Ingle and Fisher (1938) found an increase in weight of the fetal adrenals if the maternal adrenals had been removed during the pregnancy. Adrenalectomized pregnant rats delivered their litters normally, but did not lactate sufficiently to raise them unless treated with cortical hormones (Tobin, 1939). Walaas and Walaas (1944) confirmed the findings of Ingle and Fisher and showed that fetal adrenal weight increased 33% if maternal adrenals were removed on th...

ADRENAL FUNCTION IN PREMATURE INFANTS

The urinary formaldehydogenic steroid excretion was measured in 5 ACTH-treated premature infants and in 3 premature infants born of toxemic mothers. One of these toxemic mothers received no therapy, one received ACTH antepartum, and one cortisone antepartum. Na, K and N balance studies were conducted in three of the above infants. Steroid excretion rose during ACTH administration and fell 2 to 4 days after discontinuance of ACTH therapy. The fall was followed by a moderate rise, or rebound, in some cases. These findings indicate that the adrenals of young infants have a functional reserve and are capable of responding to either an increase or a decrease in the adrenocorticotrophic stimulus by a corresponding change in steroid production. This response resembles that seen in normal adults and is further evidence that this aspect of adrenal function is not impaired during involution of the fetal adrenal cortex. ACTH administration in one infant produced an increase in sodium excretion during the first 16 days of therapy. This response is the opposite of that usually found in normal adults, and confirms a similar previous finding reported by Klein. Under continued ACTH therapy, the infant ultimately retained Na as does the normal adult. The cause for this early abnormal response is unknown, but it resembles one seen in adults with Cushing's disease, in whom desoxycorticosterone induces a loss of sodium. The infant born of the cortisone-treated toxemic mother had normal postnatal urinary steroid values; the infant born of the ACTH-treated toxemic mother had unusually high postnatal values. These observations suggest that cortisone failed to cross the placenta in sufficient quantity to influence steroid excretion of the infant, but that ACTH administered to the mother reached the fetus and stimulated his adrenals.

Anaplastic cells of fetal adrenal cortex.

Journal Article Anaplastic Cells of Fetal Adrenal Cortex Get access J. M. Craig, M.D., J. M. Craig, M.D. From the Departments of Pathology, The Children’s Medical Center and Harvard Medical School, Boston, Massachusetts Search for other works by this author on: Oxford Academic Google Scholar B. H. Landing, M.D. B. H. Landing, M.D. From the Departments of Pathology, The Children’s Medical Center and Harvard Medical School, Boston, Massachusetts Search for other works by this author on: Oxford Academic Google Scholar American Journal of Clinical Pathology, Volume 21, Issue 10, 1 October 1951, Pages 940–949, https://doi.org/10.1093/ajcp/21.10.940 Published: 01 October 1951 Article history Received: 28 June 1951 Published: 01 October 1951

STEROID EXCRETION OF INFANTS

The urinary excretion of corticosteroids and ketosteroids was measured in infants during the first week of life and at four and 18 months of age. It was found that corticosteroid excretion increased with age while the excretion of ketosteroids declined from birth, but was again at a similar level to that of one-to three-day-old infants in the 18-months-old child. The excretion of androgenic substances did not parallel the excretion of ketosteroids, these substances being present in minute amounts at birth and rising gradually with increasing age. It is suggested that the involution of the fetal adrenal cortex is associated with a declining production of nonandrogenic ketosteroids.

THE EXCRETION OF NEUTRAL LIPID-SOLUBLE REDUCING SUBSTANCES BY INFANTS*

THE development of chemical methods (1, 2, 3) for the measurement of adrenocortical steroids in urine has made possible the evaluation of the level of excretion of these substances in normal individuals and in relation to diseases known to involve the adrenal cortex. A considerable amount of data is now available concerning the normal level of excretion of adrenocortical steroids by adults. Little has been done toward the determination of their elimination by infants. Knowledge of the excretory level of these compounds during the first few weeks of life may aid in explaining the function of the human fetal adrenal cortex. In order to estimate the level of excretion of adrenocortical steroids in normal infants and in the hope that these data might help toward the evaluation of the function of the fetal cortex, the amount of neutral lipid-soluble reducing substances excreted in the urine of premature and full-term infants was determined during the period when involution of the fetal cortex is known to occur.

Androgenic Assay of the Human Fetal Adrenal.

SummaryIn spite of some evidence suggesting an androgenic function of the human fetal adrenal cortex, it has not been possible to demonstrate any androgenic activity by biological assay of the tissue by a method adequate to detect as little as 10 I.U. per kilo of fresh tissue.

The early embryological development of the fetal and permanent adrenal cortex in man

The Anatomical RecordVolume 76, Issue 2 p. 183-203 Article The early embryological development of the fetal and permanent adrenal cortex in man Unto U. Uotila, Unto U. Uotila Department of Anatomy, Harvard Medical School, Boston, Massachusetts Fellow of the Rockefeller Foundation.Search for more papers by this author Unto U. Uotila, Unto U. Uotila Department of Anatomy, Harvard Medical School, Boston, Massachusetts Fellow of the Rockefeller Foundation.Search for more papers by this author First published: February 1940 https://doi.org/10.1002/ar.1090760207Citations: 50 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume76, Issue2Special Issue: Includes Annual Meeting AbstractsFebruary 1940Pages 183-203 RelatedInformation