Abstract
The cortical part of the adrenal gland is divided into three areas or zones (“zonae”); each of them produces a different steroid hormone that serves a distinct physiologic function. One of them, zona reticularis (ZR), is dedicated to the synthesis of adrenal androgens. The physiology (and pathophysiology) of the adrenal cortex is due to particular enzymes that are expressed in the different zonae; humans and other primates are unique in having infantile adrenocortical tissue that is different from that in adult life. In fetal life, very little of that compartmentalization of adrenocortical function exists; it is not until the later half of the first year of life that what we call “adult” adrenal cortex gradually occupies most of the gland. Human and primate ZR and fetal adrenal cortex (FA) produce the same steroid, dehydroepiandrosterone sulfate (DHEAS). In these species, FA provides DHEAS to the placenta to produce estrogens necessary for the maintenance of pregnancy; the need for this “placental-fetal unit” is lost at birth and the fetal zone disappears rapidly thereafter through a process of gradual adrenocortical microhemorrhages. DHEAS levels fall rapidly after birth to appear again in detectable quantities in adrenarche, rise throughout puberty, and start to fall after the age of 40 years to very low levels in late life. Sebaceous gland physiology depends on normal adrenarche and normal adrenal androgenic steroid levels; all the five major enzymes involved in the activation and deactivation of androgens are expressed in the pilosebaceous unit (PSU). Initiation of DHEAS biosynthesis early in fetal life seems to be associated with the differentiation of hairs and sebaceous glands. It has been shown that sebaceous gland function begins before true puberty, at levels of testosterone below those ordinarily required for the initiation of pubic hair growth. This development signals adrenarche, marked by increasing production of DHEAS. The levels of DHEAS have been found to correlate with sebum production in early puberty and with the presence of acne vulgaris in prepubertal children. Practically all adolescents have at least a few open and closed comedones. Persistence of acne beyond adolescence usually implies an underlying hyperandrogenemia, and a thorough work-up to rule out possible etiologies of this condition should be performed.
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Abbreviations
- ACTH:
-
Adrenocorticotropic hormone or corticotropin
- ADI:
-
5α-Androstene-3β-17b-diol
- AN:
-
Androstenedione
- CRH:
-
Corticotropin-releasing hormone
- CRH-R:
-
Corticotropin-releasing hormone receptor
- DHEA:
-
Dehydroepiandrosterone
- DHEAS:
-
Dehydroepiandrosterone sulfate
- DHT:
-
Dehydrotestosterone
- EGF:
-
Epidermal growth factor
- E2:
-
Estradiol
- FA:
-
Fetal adrenal cortex
- FGF:
-
Fibroblast growth factor
- HOX:
-
Homeobox
- IL-6:
-
Interleukin-6
- NADPH:
-
Nicotinamide adenine dinucleotide phosphate
- PCOS:
-
Polycystic ovary syndrome
- PSU:
-
Pilosebaceous unit
- P450c17:
-
17α-hydroxylase; 17,20 desmolase
- P450c11β:
-
11β-hydroxylase
- P450c21:
-
21-hydroxylase
- P450scc:
-
Cytochrome P450scc
- SF-1:
-
Steroidogenic factor 1
- StAR:
-
Steroidogenic acute regulatory protein
- T:
-
Testosterone
- TGFa:
-
Transforming growth factor a
- TGFb:
-
Transforming growth factor b
- TNF-alpha:
-
Tumor necrosis factor-alpha
- ZR:
-
Zona reticularis
- 3β-HSD:
-
3-β-Hydroxysteroid dehydrogenase
- 17β-HSD2:
-
17-β-Hydroxysteroid dehydrogenase isozyme 2
- 17β-HSD5:
-
17-β-Hydroxysteroid dehydrogenase isozyme 5
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Stratakis, C.A., Xekouki, P. (2012). Issues in Sexual Growth: The Sebaceous Glands and Adrenocortical Growth and Development. In: Preedy, V. (eds) Handbook of Growth and Growth Monitoring in Health and Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-1795-9_64
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