Borage Oil Enhances Lamellar Body Content and Alters Fatty Acid Composition of Epidermal Ceramides in Essential Fatty Acid-Deficient Guinea Pigs

Borage oil [BO: 40.9% linoleic acid (LNA) and 24.0% γ-linolenic acid (GLA)] reverses disrupted epidermal lipid barrier in essential fatty acid deficiency (EFAD). We determined the effects of BO on lamellar body (LB) content and LNA and GLA incorporation into epidermal ceramide 1 (CER1) and epidermal ceramide 2 (CER2), major barrier lipids. EFAD was induced in guinea pigs by a diet of 6% hydrogenated coconut oil (HCO) for 10 weeks (group HCO) or 8 weeks followed by 6% BO for 2 weeks (group HCO + BO). LB content and LNA and GLA incorporation into CER1 were higher in group HCO + BO than in group HCO. Small but significant levels of LNA, GLA, and their C20-metabolized fatty acids [dihomo-γ-linolenic acid (DGLA) and arachidonic acid (ARA)] were incorporated into CER2, where ARA was detected at a level lower than LNA, but DGLA incorporation exceeded that for GLA in group HCO + BO. Dietary BO enhanced LB content and differential incorporation of GLA into CER1 and DGLA into CER2.     

Mass Spectrometric Confirmation of γ-Linolenic Acid Ester-Linked Ceramide 1 in the Epidermis of Borage Oil Fed Guinea Pigs

Ceramide 1 (Cer1), a Cer species with eicosasphingenine (d20:1) amide‐linked to two different ω‐hydroxy fatty acids (C30wh:0:C32wh:1), which are, in turn, ester‐linked to linoleic acid (LNA; 18:2n‐6), plays a critical role in maintaining the structural integrity of the epidermal barrier. Prompted by the recovery of a disrupted epidermal barrier with dietary borage oil [BO: 36.5 % LNA and 23.5 % γ‐linolenic acid (GLA; 18:3n‐6)], in essential fatty acid (EFA)‐deficient guinea pigs, we further investigated the effects of BO on the substitution of ester‐linked GLA for LNA in these two epidermal Cer1 species by LC–MS in positive and negative modes. Dietary supplementation of BO for 2 weeks in EFA‐deficient guinea pigs increased LNA ester‐linked to C32wh:1/d20:1 and C30wh:0/d20:1 of Cer1. Moreover, GLA ester‐linked to C32wh:1/d20:1, but not to C30wh:0/d20:1, of Cer1 was detected, which was further confirmed by the product ions of m/z 277.2 for ester‐linked GLA and m/z 802.3 for the deprotonated C32wh:1/d20:1. C20‐Metabolized fatty acids of LNA or GLA were not ester‐linked to these Cer1 species. Dietary BO induced GLA ester‐linked to C32wh:1/d20:1 of epidermal Cer1.