Alternative method to improve the ethyl valerate yield using an immobilised Burkholderia cepacia lipase.

This study is focussed on a biocatalysing chemical synthesis in order to produce a green apple flavour (ethyl valerate) using an immobilised lipase from Burkholderia cepacia. A strategy to improve the lipase stability during the esterification is used. In order to increase the ethyl valerate efficiency, an alternative method using the buffer pH to dissolve the lipase into alginate is proposed. Parameters of the immobilised lipase such as pH, temperature, activation energy and stirring speed are evaluated. The optimal condition using the substrate concentration and the lipase loading is provided. After 5 recyclability cycles, the immobilised lipase reveals a decreasing ∼25% in the ethyl valerate yield. An economical ester synthetising associated with the esterification efficiency is evidenced. This induces that a potential industrial application can be considered. This due to the demand for ethyl valerate in the flavour industry is required.

Eicosapentaenoic acid-rich oil supplementation activates PPAR-γ and delays skin wound healing in type 1 diabetic mice.

Delayed wound healing is a devastating complication of diabetes and supplementation with fish oil, a source of anti-inflammatory omega-3 (ω-3) fatty acids including eicosapentaenoic acid (EPA), seems an appealing treatment strategy. However, some studies have shown that ω-3 fatty acids may have a deleterious effect on skin repair and the effects of oral administration of EPA on wound healing in diabetes are unclear. We used streptozotocin-induced diabetes as a mouse model to investigate the effects of oral administration of an EPA-rich oil on wound closure and quality of new tissue formed. Gas chromatography analysis of serum and skin showed that EPA-rich oil increased the incorporation of ω-3 and decreased ω-6 fatty acids, resulting in reduction of the ω-6/ω-3 ratio. On the tenth day after wounding, EPA increased production of IL-10 by neutrophils in the wound, reduced collagen deposition, and ultimately delayed wound closure and impaired quality of the healed tissue. This effect was PPAR-γ-dependent. EPA and IL-10 reduced collagen production by fibroblasts in vitro. In vivo, topical PPAR-γ-blockade reversed the deleterious effects of EPA on wound closure and on collagen organization in diabetic mice. We also observed a reduction in IL-10 production by neutrophils in diabetic mice treated topically with the PPAR-γ blocker. These results show that oral supplementation with EPA-rich oil impairs skin wound healing in diabetes, acting on inflammatory and non-inflammatory cells.