Menopause and Dermal White Adipose Tissue Depletion: Mechanistic Links, Adipogenesis, and Regenerative Therapeutic Replacement.

BACKGROUND

Menopause is linked to typical skin changes such as textural alterations, loss of skin hydration, elasticity, thinning, and increased fragility. Dermal white adipose tissue (dWAT), a distinct fat component located in the dermis and involved in hair cycle regulation, antimicrobial peptide production, and extracellular matrix (ECM) modulation, decreases with aging and photodamage. Emerging evidence suggests that estrogen contributes to an inhibitory effect on dWAT and promotes fibrotic remodeling of adipose tissue of the dermis.

OBJECTIVE

To examine the mechanistic evidence linking menopause with the loss of dWAT and to suggest and highlight potential strategies for replacing dWAT with agents such as magnolol, which promote the conversion of pre-adipocytes to adipocytes and restore lost fractions of the dWAT compartment.

METHODS

A review of the literature, a mechanistic examination, a histologic examination, and a clinical trial assessment were conducted.

RESULTS

The loss of dWAT and fibrotic replacement are likely a factor causally linked to the decrease in estrogen observed during menopause. Reduced dWAT produces fewer adipokines such as adiponectin, which is directly involved in skin health by promoting collagen and hyaluronic acid (HA) production. Evidence suggests that select non-hormonal agents can offer a potential therapeutic benefit to menopausal skin promoting dWAT restoration through adipogenic pathways.

CONCLUSION

dWAT depletion likely contributes to menopausal skin changes. Potential candidates for non-hormonal alternatives to address these menopausal concerns are discussed in this paper.