Abstract
The skin is an endocrine organ with the expression of metabolizing enzymes and hormone
receptors for diverse hormones. The sebaceous gland is the main site of hormone biosynthesis,
especially for androgens, and acne is the classical androgen-mediated dermatosis.
In sebocytes, conversion of 17-hydroxyprogesterone directly to dihydrotestosterone
bypassing testosterone has been demonstrated, while type II 17β-hydroxysteroid dehydrogenase
can inactivate the action of testosterone and dihydrotestosterone. The androgen receptor–dependent
genomic effect of dihydrotestosterone on sebocytes is confirmed. Further evidence
supports the PI3 K/Akt/FoxO1/mTOR signaling in the involvement of the interplay between
androgens, insulin, insulin-like growth factor, and hyperglycemic diet in acne. Androgens
not only regulate embryology and lipogenesis/sebum synthesis in sebocytes but also
influence inflammation in acne. Genetic studies indicate that regulation of the androgen
receptor is an important factor in severe acne. Further studies are required to understand
the effect of estrogen and progesterone on sebaceous gland and comedogenesis, considering
the change of acne in pregnancy and postmenopausal acne. Special attention should
be paid to nonobese patients with polycystic ovarian syndrome and hyperandrogenism-insulin
resistance-acanthosis nigricans syndrome. In spite of extensive gynecologic experience
in the use of combined oral contraceptives for acne, evidence based on dermatologic
observation should be intensified.
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Article info
Footnotes
Ju Q and Tao T share the first authorship.
Identification
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