Is Endogenous Glycerol a Determinant of Stratum Corneum Hydration in Humans?

Abstract

Although stratum corneum (SC) hydration has been primarily of concern to the cosmetic industry, it serves an important biosensor function. In murine models, not only deiminated products of filaggrin-derived amino acids ("NMF") but also endogenous glycerol from circulation into the epidermis via aquaporin 3 channel and from triglyceride turnover in sebaceous glands (SG) are important determinants. We assessed here whether endogenous glycerol could also be linked to SC hydration in humans. SG-enriched sites are more hydrated than SG-impoverished sites, and SC hydration correlates with both sebum production and SC glycerol content, but the correlation is more significant for SC glycerol content than for sebum content. Moreover, gender-related differences in sebum content are not associated with altered SC hydration. SC hydration is also linked to SC glycerol content in SG-impoverished sites, suggesting a role for non-SG-derived (? from circulation) glycerol in SC hydration. Finally, short-term water immersion produces a parallel decline in SC hydration and SC glycerol content, with glycerol levels returning to normal over several hours. These results suggest that endogenous glycerol of both circulatory and SG origin comprises an H2O-extractable pool that influences SC hydration in humans. These results also provide a rationale for the development of glycerol-containing therapeutic moisturizers.

The determination of stratum corneum thickness An alternative approach

“…These loose portions seem to constitute a minor barrier to water loss, but do represent a considerable mass when removed. This agrees with the heterogeneous nature of the SC structure [18][19][20][21]; where the SC compactum evolves into the SC disjunctum as the corneocytes migrate towards the surface, and progressively loose their corneodesmosome links. The cells of the SC disjunctum do not contribute significantly to the water barrier function of the SC.…”

“…(3) yields an initial plateau followed by a declining straight line. It could be hypothesized that this initial plateau corresponds to the removal of the stratum corneum disjunctum; the looser outer stratum corneum layer [18][19][20][21] which does not provide a significant contribution to the barrier to water loss. It follows that its removal would contribute a significant mass change without a corresponding increase in TEWL.…”

Thematic review series: Skin Lipids. The role of epidermal lipids in cutaneous permeability barrier homeostasis

“…However, in animals deficient in SCD1 (asebia mice), there are no abnormalities in permeability barrier homeostasis (SCD1-deficient mice have a sebaceous gland defect that will be discussed in Diane Thiboutot's review in this series) (92). The absence of defects in permeability barrier function in asebia mice that have marked abnormalities in sebaceous glands and the presence of normal permeability barrier function in areas of human skin with a paucity of sebaceous glands indicate that the lipids produced by sebaceous glands are not essential for permeability barrier homeostasis (92,93). However, stratum corneum hydration is decreased in asebia mice that are deficient in sebaceous glands and in areas of human skin with a decreased number of sebaceous glands (92,93).…”

“…The absence of defects in permeability barrier function in asebia mice that have marked abnormalities in sebaceous glands and the presence of normal permeability barrier function in areas of human skin with a paucity of sebaceous glands indicate that the lipids produced by sebaceous glands are not essential for permeability barrier homeostasis (92,93). However, stratum corneum hydration is decreased in asebia mice that are deficient in sebaceous glands and in areas of human skin with a decreased number of sebaceous glands (92,93). The triglycerides in sebaceous lipids are metabolized by lipases to free fatty acids and glycerol, and a decrease in glycerol in areas with reduced sebaceous gland activity leads to a decrease in stratum corneum hydration (92,93).…”

Effect of retinoic acid on aquaporin 3 expression in keratinocytes

“…Eleven types of AQPs have been discovered in the human body thus far. They exist not only in the ependyma, heart, alveoli, biliary system, kidney, lens internal capsule, exocrine gland epithelial cells, and some organs involved with metal and water metabolism, but also in the keratinocyte membrane of the epidermis (Choi et al, 2005;Olsson et al, 2006;Qi et al, 2009). Several references have already confirmed that AQP3 plays an important role in the recovery of skin barrier functions (Sugiyama et al, 2001;Roudier et al, 2002;Boury-Jamot et al, 2006).…”