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Testosterone perturbs epidermal permeability barrier homeostasis
1Dermatology & Medical Services (Metabolism), VAMC, Department of Dermatology , UCSF, San Francisco, California, USA.
The Journal of Investigative Dermatology
|March 7, 2001
Summary
Testosterone slows skin barrier recovery in adult mice and humans. Lowering testosterone levels or blocking its effects accelerates barrier repair by impacting epidermal lamellar body formation and secretion.
Area of Science:
- Dermatology
- Endocrinology
- Skin Physiology
Background:
- While adult skin barrier function shows no gender differences, fetal skin development is sexually dimorphic.
- Estrogens accelerate, while testosterone retards, fetal skin barrier development.
- Androgen receptor antagonists normalize developmental rates in male and female fetuses.
Purpose of the Study:
- To investigate the effects of testosterone on skin barrier homeostasis in adult animals and humans.
- To understand the mechanisms underlying testosterone's influence on skin barrier function.
Main Methods:
- Utilized hypogonadal mice (castrated or flutamide-treated) and normal mice.
- Administered systemic and topical flutamide (androgen receptor antagonist).
- Examined barrier recovery rates, epidermal lipid synthesis, and lamellar body (LB) formation/secretion.
- Correlated barrier recovery with testosterone levels in a human subject.
Main Results:
- Hypogonadal mice exhibited significantly faster skin barrier recovery than controls.
- Testosterone replacement slowed barrier recovery in castrated mice.
- Topical flutamide accelerated barrier recovery in normal male mice.
- Reduced LB formation and secretion were observed in testosterone-replete animals, leading to fewer extracellular lamellar bilayers.
Conclusions:
- Testosterone modulates skin permeability barrier function in adult mammals.
- Elevated testosterone levels impair skin barrier recovery.
- Reduced lamellar body secretion is a key mechanism for testosterone-induced barrier dysfunction.