Endocrine - Adrenal Development

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Introduction

Adrenal Gland (week 10)

The developing adrenal gland has both an interesting origin and an intruiging fetal role. Furthermore recent studies suggest that the adrenal cortex share a common embryonic origin with the early gonad. The adrenal gland and placenta also act in synergy, and the notes endocrine placenta should also be read.


The 2 adrenal glands (suprarenal gland, glandulæ suprarenales) are named by their anatomical postion sitting above the 2 kidneys (renal). The 2 main parts of the adrenals have different embryonic origins. The inside core adrenal medulla is neural crest in origin. Mesenchyme surrounding these cells differentiates to form a fetal cortex. This fetal cortex is later replaced by the adult cortex. The outside adrenal cortex is derived from mesothelium and can be further divided into 3 distinct layers (zona reticularis, zona fasiculata, zona glomerulosa) each with distinct hormonal functions.


During fetal development, adrenal hormones are involved with production of precursor for placental estrogen production, ovary and brain development, the maturation of the lung and other developing systems.

Links: neural crest | Endocrine Lecture | Lecture - Neural Crest Development


Historic Embryology - Adrenal  
1912 Suprarenal Bodies | 1914 Suprarenal Organs | 1920 Adrenal | 1940 Adrenal | 1957 Adrenal


Endocrine Links: Introduction | BGD Lecture | Science Lecture | Lecture Movie | pineal | hypothalamus‎ | pituitary | thyroid | parathyroid | thymus | pancreas | adrenal | endocrine gonad‎ | endocrine placenta | other tissues | Stage 22 | endocrine abnormalities | Hormones | Category:Endocrine
Historic Embryology - Endocrine  
1903 Islets of Langerhans | 1903 Pig Adrenal | 1904 interstitial Cells | 1908 Pancreas Different Species | 1908 Pituitary | 1908 Pituitary histology | 1911 Rathke's pouch | 1912 Suprarenal Bodies | 1914 Suprarenal Organs | 1915 Pharynx | 1916 Thyroid | 1918 Rabbit Hypophysis | 1920 Adrenal | 1935 Mammalian Hypophysis | 1926 Human Hypophysis | 1927 Adrenal | 1927 Hypophyseal fossa | 1930 Adrenal | 1932 Pineal Gland and Cysts | 1935 Hypophysis | 1935 Pineal | 1937 Pineal | 1935 Parathyroid | 1940 Adrenal | 1941 Thyroid | 1950 Thyroid Parathyroid Thymus | 1957 Adrenal

Some Recent Findings

  • Adrenal gland size in growth restricted fetuses[1] "To compare the adrenal gland size of fetal growth restricted (FGR) and normal control fetuses. ... The adrenal gland cortex width and the adrenal gland ratio were increased in FGR fetuses compared to normal fetuses." ultrasound
  • Multipotent peripheral glial cells generate neuroendocrine cells of the adrenal medulla[2] "We demonstrate that large numbers of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs). SCPs migrate along the visceral motor nerve to the vicinity of the forming adrenal gland, where they detach from the nerve and form postsynaptic neuroendocrine chromaffin cells."
  • Fetal adrenal gland in the second half of gestation: morphometrical assessment with 3.0T post-mortem MRI[3] "The morphometry of fetal adrenal gland is rarely described with MRI of high magnetic field. The purpose of this study is to assess the normal fetal adrenal gland length (AL), width (AW), height (AH), surface area (AS) and volume (AV) in the second half of gestation with 3.0T post-mortem MRI. Fifty-two fetal specimens of 23-40 weeks gestational age (GA) were scanned by 3.0T MRI. Morphological changes and quantitative measurements of the fetal adrenal gland were analyzed. Asymmetry and sexual dimorphism were also obtained. The shape of the fetal adrenal gland did not change substantially from 23 to 40 weeks GA. The bilateral adrenal glands appeared as a 'Y', pyramidal or half-moon shape after reconstruction. There was a highly linear correlation between AL, AW, AH, AS, AV and GA. AW, AH, AS and AV were larger for the left adrenal gland than the right. No sexual dimorphism was found." magnetic resonance imaging
More recent papers  
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Older papers  
  • A morphometric study of suprarenal gland development in the fetal period[4] "This study was performed on 172 human fetuses (76 males and 96 females) and 344 fetal suprarenal glands obtained from ages 9-40 weeks of gestation with no external pathology or anomaly. It is found that all parameters increase with gestational age. There was significant correlation between gestational age and all parameters (p < 0.001). No significant differences were observed between sexes for any of the parameters (p > 0.05). There was no difference between the right and left sides of parameters except the thickness of the suprarenal glands. The left suprarenal glands were thicker than the right. The ratio of suprarenal volumes to kidney volumes was determined, and we observed that the ratio decreased during the fetal period."
  • Migration and distribution of neural crest-derived cells in the human adrenal cortex at 9-16 weeks of gestation[5] "In sagittal as well as horizontal sections of human fetuses between 9 and 16 weeks of gestation, we identified chromaffin, ganglion and Schwann-like cells in the developing adrenal gland using immunohistochemistry. Cells showing tyrosine hydroxylase (TH) immunoreactivity (i.e., candidate ganglion cells) entered the fetal cortex mainly from the medial half of the adrenal, but the path of entry also included the ventral, dorsal and caudal aspects. ...The entry of neural crest-derived cells does not appear to be restricted to a hypothetical medial hilus, but occurs widely around the cortex, with or without the accompaniment of Schwann-like cells. These cells advance in lines through the fetal cortex in a cord-like arrangement without destruction of the cortical architecture. Some of the TH-positive cells very likely express chromogranin A before entry into the adrenal."
  • Development of the human adrenal zona reticularis: morphometric and immunohistochemical studies from birth to adolescence.[6] "Results demonstrated that ZR became discernible around 4 years of age, and both thickness and ratio per total cortex of ZR increased in an age-dependent fashion thereafter, although there was no significant increment in total thickness of developing adrenal cortex. We further evaluated immunoreactivity of both KI67 and BCL2 in order to clarify the equilibrium between cell proliferation and apoptosis in the homeostasis of developing human adrenals. Results demonstrated that proliferative adrenocortical cells were predominantly detected in the zona glomerulosa and partly in outer zona fasciculata (ZF) before 4 years of age and in ZR after 4 years of age, but the number of these cells markedly decreased around 20 years of age."
  • Development and Function of the Human Fetal Adrenal Cortex: A Key Component in the Feto-Placental Unit[7] "The steroidogenic activity is characterized by early transient cortisol biosynthesis, followed by its suppressed synthesis until late gestation, and extensive production of dehydroepiandrosterone and its sulfate, precursors of placental estrogen, during most of gestation. The gland rapidly grows through processes including cell proliferation and angiogenesis at the gland periphery, cellular migration, hypertrophy, and apoptosis." (See also Fetal Development)

Adrenal Movies

Adrenal medulla.jpg
 ‎‎Adrenal Medulla
Page | Play
Human fetal adrenal GA32.jpg
 ‎‎Adrenal GA32
Page | Play
Cartoon showing migration of neural crest cells
from original location to form the fetal medulla cells.
Surface rendering of human fetal adrenal glands
in the third trimester (week 30 GA week 32).

Adrenal Overview

  • Richly vascularized - arterioles passing through cortex, capillaries from cortex to medulla, portal-like circulation
  • Fetal Cortex - produces a steroid precursor (DEA), converted by placenta into estrogen
  • Adult Medulla - produces adrenalin (epinephrine), noradrenaline (norepinephrine)
  • Fetal adrenal hormones - influence lung maturation

Cortical Hormones

(steroids) Cortisol, Aldosterone, Dehydroepiandrosterone

  • zona glomerulosa - regulated by renin-angiotensin-aldosterone system controlled by the juxtaglomerular apparatus of the kidney.
  • zona fasciculata - regulated by hypothalamo-pituitary axis with the release of CRH and ACTH respectively.

Medullary Hormones

(amino acid derivatives) Epinephrine, Norepinephrine

Adrenal Development

Adrenal gland development and steroid hormone synthesis
Fetal adrenal gland steroidogenesis.jpg
Overview cartoon of changes in adrenal gland structure and steroid hormone syntesis[8]
Ontogenesis of steroidogenic enzymes in the human fetal adrenal gland. This schematic representation is divided into portions showing the fetal adrenal gland (right) at the first, second and third trimesters of pregnancy, and the adult adrenal gland (left). During the first trimester, the fetal gland is composed of a definitive zone (DZ, light grey) and a fetal zone (FZ, dark grey).

Fetal zone (FZ) - expressing the P450C17 cytochrome, is responsible for massive secretion of DHEA and DHEA/S, used by the placenta as estrogen precursors.

Second trimester - chromaffin cells (CC, black) originating from the neural crests migrate through the fetal cortex to progressively colonize the center of the gland to form the future medulla (Med).

Third trimester - the newly constituted transitional zone (TZ, medium grey) acquires the enzyme 3ß-HSD while the expression of P450C17 remains, thus allowing the production of fetal cortisol. Near birth, cells of the definitive zone which express only 3ß-HSD, acquire the P450aldo and begin to secrete mineralocorticoids such as aldosterone.

Neonatal - the fetal adrenal regresses strongly (mainly due to the regression of the fetal zone) and recovers progressively during the first years of extra-uterine life.

Adult - adult adrenal gland is composed of the zona glomerulosa (ZGlo, light grey), zona fasciculata (ZFasc , medium grey) and zona reticularis (ZRet, dark grey) responsible for the production of mineralocorticoids (aldosterone), glucocorticoids (cortisol) and androgens (DHEA-DHEA/S), respectively.

{based on data from PMID 9183569)

  • P450scc - cytochrome P450 side chain cleavage
  • Pregn. - pregnenolone
  • P450C17 - cytochrome P450 17a-hydroxylase, 17-20 lyase
  • 17OHP5 - 17-hydroxy-pregnenolone
  • DHEA/S - dehydroepiandrosterone-sulfate
  • S-Tfase - DHEA sulfotransferase
  • 3ß-HSD - 3ß-hydroxysteroid dehydrogenase
  • Prog. - progesterone
  • 17OHP4 - 17-hydroxyprogesterone
  • P450C21 - cytochrome P450 21-hydroxylase
  • P450C11 - cytochrome P450 11ß-hydroxylase
  • P450aldo - cytochrome P450 aldosterone synthase.
  • Fetal Adrenals - fetal cortex later replaced by adult cortex
  • Week 6 - fetal cortex, from mesothelium adjacent to dorsal mesentery; Medulla, neural crest cells from adjacent sympathetic ganglia
  • Adult cortex - mesothelium mesenchyme encloses fetal cortex

Adrenal Cortex

  • Late Fetal Period - differentiates to form cortical zones
  • Birth - zona glomerulosa, zona fasiculata present
  • Year 3 - zona reticularis present

Adrenal Medulla

  • neural crest origin, migrate adjacent to coelomic cavity, initially uncapsulated and not surrounded by fetal cortex, cells have neuron-like morphology
  • 2 cell types - secrete epinepherine (adrenaline) 80%; secrete norepinepherine (noradrenaline* 20%
Adrenal medulla.jpg
 ‎‎Adrenal Medulla
Page | Play
Week 10 adrenal gland
Human fetal adrenal gland 01.jpg
Human fetal adrenal gland morphology and size.[3]
Links: Endocrinology - Adrenal Cortex Development

Development Overview

Medulla - Neural crest cells migrate toward the coelomic cavity wall and form the adrenal medulla. These chromaffin (chromaphil) cells originally named because of their staining (yellow) with chromium salts.

Cortex - Week 4 celomic epithelium (mesothelium) cells proliferate initially forming small buds that separate from the epithelium. Week 6 these now mesenchymal cells first form the fetal adrenal cortex which will be later replaced by the adult cortex.

Adrenal Cortex

Adrenal gland (Mouse E16.5)
Human-adrenal gland 01.jpg Week10 adrenal.jpg
Human Embryo (8 weeks, stage 22) adrenal gland showing the fetal and permanent adrenal cortex. Note that the medulla of the adrenal gland is not yet encapsulated by the cortex. Human Fetus (10 week, 40mm, parasagittal section) shows location of the developing adrenal gland. The spongy appearance at the centre of the adrenal is the degenerating fetal cortex. The dense region around the outside of the adrenal is the developing adult cortex.)

Week 4 - coelomic epithelium (mesothelium) cells proliferate initially forming small buds that separate from the epithelium.

Week 6 - these now mesenchymal cells surrounding the developing medulla cells differentiate first form the fetal adrenal cortex which will be later replaced by the adult cortex.

Week 8 to 9 - fetal adrenal cortex synthesizes cortisol and is maximal at 8-9 weeks post conception (wpc) under the regulation of ACTH (also stimulates androstenedione and testosterone secretion).[9]

Adult cortex - mesothelium mesenchyme encloses fetal cortex.

Late Fetal Period - differentiates to form cortical zones.

Birth - zona glomerulosa, zona fasiculata present.

Year 3 - zona reticularis present.

Fetal Cortex

Fetal Cortex (week 12)

Fetal adrenal cortical growth involves several cellular processes: hypertrophy, hyperplasia, apoptosis, and migration.

In the second and third trimesters a steroid precursor dehydroepiandrosterone (DHEA) and sulphated derivative (DHEAS) which is converted by placenta into estrogen.

Three functional zones:

  1. Fetal zone - throughout gestation expresses enzymes required for DHEA-S synthesis.
  2. Transitional zone - initially identical to the fetal zone but later (after 25-30 weeks) expresses enzymes that suggest glucocorticoid synthesis.
  3. Definitive zone - after 22-24 weeks expresses enzymes that suggest mineralocorticoid synthesis.


Neonatal

  • human males produce high levels of DHEA) and DHEAS
  • decline within a few months of birth
  • due to regression of the adrenal fetal zone

Adult

  • zona reticularis (ZR) source for production of DHEA and DHEAS

Adult Cortex

Endocrine pathway: Hypothalamus-Pituitary-Adrenal

Development of the early adult cortex (Fetal week 12)

Early Adult Cortex (week 12)

  • Reticularis - narrow band, many small cells and capillaries androgens. source for production of DHEA and DHEAS
  • Fasiculata - high lipid content, pale foamy cells cortisol, corticosterone, cortisone.
  • Glomerulosa - small cells, cords or oval groups, aldosterone.

Species Difference

  • rat - zona glomerulosa and zona fasciculata separated by an undifferentiated zone (ZU, or Zona Intermedia)
  • mouse - no undifferentiated zone separation.
    • capsule mesenchyme cells have properties of adrenocortical stem/progenitor cells.

Adult Histology

Adrenal Histology: Cortex and Medulla | Unlabelled Overview | Cortical Zones | Zona Glomerulosa and Fasciculata | Zona Glomerulosa | Zona Fasciculata | Zona Reticularis and Medulla | Zona Reticularis | Medulla | Fetal Cortex | Developing Adult Cortex | BGD - Endocrine Histology | Histology Stains | Adrenal Development

Molecular

Steroidogenic Factor 1

Adrenal and gonad steroidogenic factor 1 expression.jpg

Adrenal and gonad steroidogenic factor 1 (SF-1) expression in different species [10]

  • 53 kDa protein called Ad4BP (Adrenal 4 Binding Protein) or SF-1 (Steroidogenic Factor 1)
  • classical DNA-binding domain (DBD) characterized by two Cys2-Cys2 zinc fingers in the N-terminal region
  • SF-1 binds DNA as a monomer
  • high homology with the drosophila Ftz-F1 transcription factor that controls fushi tarazu homeotic gene expression

Steroidogenic Factor 1 Mutation Effects

Organism
Mouse
Human
Genotype SF-1 -/- SF-1 +/- SF-1 -/+ or SF-1 -/-
Adrenal Agenesis Histological defects

Hyporesponse to stress

Compensatory growth defects

Insufficiency (agenesis or dysgenesis)
Testis Agenesis

Sex reversal

Sex reversal
Ovary Agenesis Normal
Ventro-Medial Hypothalamus Agenesis

Obesity caused by absence of the VMH (8 weeks)

Pituitary Defects of gonadotrope cells

Table modified from review.[10]

SoxE

Sry-box (Sox) 8, and Sox10 are expressed in the neural crest and in neural crest cells migrating to the adrenal gland.[11]

DAX1

CYP17

Abnormalities

Congenital Adrenal Hyperplasia

The adrenal abnormality of congenital adrenal hyperplasia (CAH) is a family of inherited disorders of adrenal steroidogenesis enzymes which impairs cortisol production by the adrenal cortex.

Enzymes most commonly affected: 21-hydroxylase (21-OH), 11beta-hydroxylase, 3beta-hydroxysteroid dehydrogenase.

Enzymes less commonly affected: 17 alpha-hydroxylase/17,20-lyase and cholesterol desmolase.

Classical CAH - androgen excess leads newborn females with external genital ambiguity and postnatal progressive virilization in both sexes.

Congenital Adrenal Hyperplasia
Type Enzyme Deficiency Female Male
classic virilizing adrenal hyperplasia 21-hydroxylase, 11-beta-hydroxylase,
or 3-beta-hydroxysteroid dehydrogenase
ambiguous genitalia at birth - complete or partial fusion of the labioscrotal folds and a phallic urethra to clitoral enlargement (clitoromegaly), partial fusion of the labioscrotal folds, or both normal genitalia, present at age 1-4 weeks with salt wasting (classic salt-wasting adrenal hyperplasia)
simple virilizing adrenal hyperplasia mild 21-hydroxylase identified later in childhood because of precocious pubic hair, clitoral enlargement (clitoromegaly), or both, often accompanied by accelerated growth and skeletal maturation early genital development (pubic hair and/or phallic enlargement) accelerated growth and skeletal maturation
nonclassic adrenal hyperplasia milder deficiencies of 21-hydroxylase
or 3-beta-hydroxysteroid dehydrogenase
present at puberty or adult with infrequent menstruation (oligomenorrhea), abnormal hair growth (hirsutism), and/or infertility
17-hydroxylase deficiency syndrome 17-hydroxylase deficiency or

3-beta-hydroxysteroid dehydrogenase

rare, phenotypically female at birth do not develop breasts or menstruate in adolescence and may have hypertension steroidogenic acute regulatory (StAR) deficiency have ambiguous genitalia or female genitalia, at puberty may lack breast development and may have hypertension
This is a complex steroidogenic abnormality, and the above table of clinical descriptions are provided only a guide.
Links: Genital Abnormalities | Adrenal Development | Genes and Disease | OMIM 21 Deficiency | OMIM 17 Deficiency | OMIM 3 Deficiency
Links: genital abnormalities

Pheochromocytomas

(PCC) Catecholamine-producing (neuro)endocrine tumor located in the adrenal medulla. Similar catecholamine-producing tumors outside the adrenal gland are called paragangliomas (PGL).

Cushing's Syndrome

(hypercortisolism) A relatively rare metabolic hormonal disorder caused by prolonged exposure of the body’s tissues to high levels of the adrenal hormone cortisol, most commonly affects adults aged between 20 to 50 and also the obese with type 2 diabetes.

Links: NIH National Endocrine and Metabolic Diseases - Cushing’s Syndrome

Adrenocortical Tumour

Childhood adrenocortical tumours distribution by age and gender (n=125)[12]

Adrenocortical tumours (ACT) can occur at all ages and have a bimodal distribution with peaks of incidence at about 5 years of age and again at 40 to 50 years of age. Clinically, a routine hormonal profile for suspected patients includes measurements of serum (8am, 11pm) cortisol, testosterone, DHEA-S, androstenedione, 17-hydroxyprogesterone, aldosterone, and plasma renin activity.[12]

References

  1. Heese S, Hammer K, Möllers M, Köster HA, Falkenberg MK, Eveslage M, Braun J, Oelmeier de Murcia K, Klockenbusch W & Schmitz R. (2018). Adrenal gland size in growth restricted fetuses. J Perinat Med , , . PMID: 29543592 DOI.
  2. Furlan A, Dyachuk V, Kastriti ME, Calvo-Enrique L, Abdo H, Hadjab S, Chontorotzea T, Akkuratova N, Usoskin D, Kamenev D, Petersen J, Sunadome K, Memic F, Marklund U, Fried K, Topilko P, Lallemend F, Kharchenko PV, Ernfors P & Adameyko I. (2017). Multipotent peripheral glial cells generate neuroendocrine cells of the adrenal medulla. Science , 357, . PMID: 28684471 DOI.
  3. 3.0 3.1 Zhang Z, Meng H, Hou Z, Ma J, Feng L, Lin X, Tang Y, Zhang X, Liu Q & Liu S. (2013). Fetal adrenal gland in the second half of gestation: morphometrical assessment with 3.0T post-mortem MRI. PLoS ONE , 8, e75511. PMID: 24116052 DOI.
  4. Ozgüner G, Sulak O & Koyuncu E. (2012). A morphometric study of suprarenal gland development in the fetal period. Surg Radiol Anat , 34, 581-7. PMID: 22430763 DOI.
  5. Inoue S, Cho BH, Song CH, Fujimiya M, Murakami G & Matsubara A. (2010). Migration and distribution of neural crest-derived cells in the human adrenal cortex at 9-16 weeks of gestation: an immunohistochemical study. Okajimas Folia Anat Jpn , 87, 11-6. PMID: 20715567
  6. Hui XG, Akahira J, Suzuki T, Nio M, Nakamura Y, Suzuki H, Rainey WE & Sasano H. (2009). Development of the human adrenal zona reticularis: morphometric and immunohistochemical studies from birth to adolescence. J. Endocrinol. , 203, 241-52. PMID: 19723922 DOI.
  7. Ishimoto H & Jaffe RB. (2011). Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit. Endocr. Rev. , 32, 317-55. PMID: 21051591 DOI.
  8. Chamoux E, Otis M & Gallo-Payet N. (2005). A connection between extracellular matrix and hormonal signals during the development of the human fetal adrenal gland. Braz. J. Med. Biol. Res. , 38, 1495-503. PMID: 16172742 DOI.
  9. Goto M, Piper Hanley K, Marcos J, Wood PJ, Wright S, Postle AD, Cameron IT, Mason JI, Wilson DI & Hanley NA. (2006). In humans, early cortisol biosynthesis provides a mechanism to safeguard female sexual development. J. Clin. Invest. , 116, 953-60. PMID: 16585961 DOI.
  10. 10.0 10.1 Val P, Lefrançois-Martinez AM, Veyssière G & Martinez A. (2003). SF-1 a key player in the development and differentiation of steroidogenic tissues. Nucl. Recept. , 1, 8. PMID: 14594453 DOI.
  11. Reiprich S, Stolt CC, Schreiner S, Parlato R & Wegner M. (2008). SoxE proteins are differentially required in mouse adrenal gland development. Mol. Biol. Cell , 19, 1575-86. PMID: 18272785 DOI.
  12. 12.0 12.1 Marques-Pereira R, Delacerda L, Lacerda HM, Michalkiewicz E, Sandrini F & Sandrini R. (2006). Childhood adrenocortical tumours: a review. Hered Cancer Clin Pract , 4, 81-9. PMID: 20223012 DOI.

Online Textbooks

Endocrinology: An Integrated Approach Nussey, S.S. and Whitehead, S.A. Oxford, UK: BIOS Scientific Publishers, Ltd; 2001. 4.7. Embryology of the adrenal gland | The Adrenal Gland | Anatomical and functional zonation in the adrenal cortex

Developmental Biology (6th ed) Gilbert, Scott F. Sunderland (MA): Sinauer Associates, Inc.; c2000. Figure 13.6. Final differentiation of a trunk neural crest cell committed to become either an adrenomedullary (chromaffin) cell or a sympathetic neuron

Molecular Biology of the Cell (4th Edn) Alberts, Bruce; Johnson, Alexander; Lewis, Julian; Raff, Martin; Roberts, Keith; Walter, Peter. New York: Garland Publishing; 2002. table 15-1. Some Hormone-induced Cell Responses Mediated by Cyclic AMP | Cells Can Respond Abruptly to a Gradually Increasing Concentration of an Extracellular Signal

Health Services/Technology Assessment Text (HSTAT) Bethesda (MD): National Library of Medicine (US), 2003 Oct. Adrenal Gland search Results

Search NLM Online Textbooks- "adrenal development" : Endocrinology | Molecular Biology of the Cell | The Cell- A molecular Approach

Reviews

Asby DJ, Arlt W & Hanley NA. (2009). The adrenal cortex and sexual differentiation during early human development. Rev Endocr Metab Disord , 10, 43-9. PMID: 18670886 DOI.

Ferraz-de-Souza B & Achermann JC. (2008). Disorders of adrenal development. Endocr Dev , 13, 19-32. PMID: 18493131 DOI.

Hanley NA & Arlt W. (2006). The human fetal adrenal cortex and the window of sexual differentiation. Trends Endocrinol. Metab. , 17, 391-7. PMID: 17046275 DOI.

Huber K. (2006). The sympathoadrenal cell lineage: specification, diversification, and new perspectives. Dev. Biol. , 298, 335-43. PMID: 16928368 DOI.

Yanase T, Gondo S, Okabe T, Tanaka T, Shirohzu H, Fan W, Oba K, Morinaga H, Nomura M, Ohe K & Nawata H. (2006). Differentiation and regeneration of adrenal tissues: An initial step toward regeneration therapy for steroid insufficiency. Endocr. J. , 53, 449-59. PMID: 16807499

Jaffe RB, Mesiano S, Smith R, Coulter CL, Spencer SJ & Chakravorty A. (1998). The regulation and role of fetal adrenal development in human pregnancy. Endocr. Res. , 24, 919-26. PMID: 9888597

Mesiano S & Jaffe RB. (1997). Developmental and functional biology of the primate fetal adrenal cortex. Endocr. Rev. , 18, 378-403. PMID: 9183569 DOI.

Articles

Speiser PW. (2010). Growth and development: congenital adrenal hyperplasia-glucocorticoids and height. Nat Rev Endocrinol , 6, 14-5. PMID: 20010965 DOI.

Hui XG, Akahira J, Suzuki T, Nio M, Nakamura Y, Suzuki H, Rainey WE & Sasano H. (2009). Development of the human adrenal zona reticularis: morphometric and immunohistochemical studies from birth to adolescence. J. Endocrinol. , 203, 241-52. PMID: 19723922 DOI.

Val P, Martinez-Barbera JP & Swain A. (2007). Adrenal development is initiated by Cited2 and Wt1 through modulation of Sf-1 dosage. Development , 134, 2349-58. PMID: 17537799 DOI.

Goto M, Piper Hanley K, Marcos J, Wood PJ, Wright S, Postle AD, Cameron IT, Mason JI, Wilson DI & Hanley NA. (2006). In humans, early cortisol biosynthesis provides a mechanism to safeguard female sexual development. J. Clin. Invest. , 116, 953-60. PMID: 16585961 DOI.

Villa-Cuesta E & Modolell J. (2005). Mutual repression between msh and Iro-C is an essential component of the boundary between body wall and wing in Drosophila. Development , 132, 4087-96. PMID: 16093324 DOI.

Boglione L, Bondone C, Corno E, Gastaldo L, Borghi F, Gattolin A & Levi AC. (2001). The development of the suprarenal gland: surgical and anatomical considerations. Panminerva Med , 43, 33-7. PMID: 11319516

Jaffe RB, Mesiano S, Smith R, Coulter CL, Spencer SJ & Chakravorty A. (1998). The regulation and role of fetal adrenal development in human pregnancy. Endocr. Res. , 24, 919-26. PMID: 9888597

"The rapid growth of the human fetal adrenal gland, which is primarily a reflection of the growth of the unique fetal zone, is regulated by ACTH acting indirectly to stimulate the expression of locally produced growth factors, of which IGF-II and bFGF appear to play key roles. Through most of gestation, the outer definitive zone appears to function as a reservoir of progenitor cells which move centripetally to populate the rest of the gland. At the end of pregnancy, the fetal zone undergoes senescence through an apoptotic process. Activin and TGF-beta are capable of inducing apoptosis in the fetal zone. Corticotropin-releasing hormone, which is produced by the placenta in markedly increased amounts at the end of gestation, may orchestrate a variety of processes, including direct stimulation of fetal adrenal steroidogenesis, culminating in the initiation of parturition."

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Cite this page: Hill, M.A. (2024, March 29) Embryology Endocrine - Adrenal Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Endocrine_-_Adrenal_Development

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