We examined the effect of oral intake of pure glucosylceramide derived from konjac extract on skin barrier function evaluated by transepidermal water loss (TEWL) in hairless mice with sodium dodecyl sulfate (SDS)-induced skin roughness. The difference of TEWL between SDS-treated site and untreated sites in the pure glucosylceramide-fed group was significantly lower than that in control group on day 14 of ingestion. We investigated interleukin-1α (IL-1α) production in the hairless mouse skin, and it was significantly lower in the glucosylceramide-fed group than that of control animals. This reduced IL-1α production should contribute to improvement of skin barrier function. To investigate the effect of oral intake of glucosylceramide in human, we conducted a randomized double-blind placebo-controlled study including 100 healthy subjects whose TEWL in cheek was relatively high. As a result, cheek TEWL was significantly lower in the test product group as compared with the control group in weeks 8 and 12 of ingestion (p = 0.023 and p = 0.002 respectively).
In this study, we investigated whether dietary glucosylceramide (GlcCer) and its metabolite sphingoid bases, sphingosine (SS), phytosphingosine (PS), sphingadienine (SD) and 4-hydroxysphingenine (4HS), influence cornified envelope (CE) formation. CE is formed during terminal differentiation of the epidermis through crosslinking of specific precursor proteins by transglutaminases (TGases), and is essential for the skin's barrier function. Oral administration of GlcCer (0.25 mg/day) for 14 consecutive days dramatically reduced transepidermal water loss, an indicator of the skin barrier condition, in hairless mice with barrier perturbation induced by single-dose ultraviolet B (UVB) irradiation. The GlcCer treatment also increased the level of TGase-1 mRNA in UVB-irradiated murine epidermis approximately 1.6-fold compared with the control. Further, all four sphingoid bases at 1 μM concentration enhanced CE formation of cultured normal human keratinocyte cells. Among them, SS, PS and SD, but not 4HS, stimulated production of involucrin, one of the CE major precursor proteins. SD increased the expression of TGase-1 mRNA, while SS increased the expression of TGase-3 mRNA. These results indicate that the skin barrier improvement induced by oral GlcCer treatment might be at least partly due to a reinforcement of CE formation in the epidermis mediated by sphingoid bases metabolically derived from GlcCer.
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