Thus, the objective of this study was to develop an inducible transgenic mouse model for the synthesis of n-3 PUFA. No experimental model currently exists which enables the precise study of timing of exposure of n-3 PUFA. In particular, timing of exposure during the lifecycle is becoming increasingly salient as a growing body of research suggests that the origins of chronic disease begins in the early years of life (Calkins and Devaskar 2011). However, there remain many fundamental questions regarding their biological role and mechanism of action. Introduction In recent years, dietary n-3 PUFA, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have garnered strong research and public interest due to their numerous reported beneficial health effects (Anderson and Ma 2009 Fetterman and Zdanowicz 2009).
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elegans Caenorhabditis elegans Hprt Hypoxanthine phosphoribosyltransferase HAT Hypoxanthine, aminopterin and thymidine PEI Polyethylenimine LA Linoleic acid IP Intraperitoneal PE Phosphatidylethanolamine PC Phosphatidylcholine PS Phosphatidylserine PI Phosphatidylinositol ALA a-Linolenic acid SFA Saturated fatty acid MUFA Monounsaturated fatty acid 4-OHT 4-Hydroxytamoxifen
Keywords fat-1 n-3 Desaturase Cre-recombinase loxP Abbreviations HEK Human embryonic kidney EPA Eicosapentaenoic acid DHA Docosahexaenoic acid C. Collectively these findings suggest that the iFat1 transgenic mouse may be a promising tool to help elucidate the temporal effects through which n-3 PUFA impacts health related outcomes. (p \ 0.05) tissue n-3 PUFA and Ctwo-fold reduction (p \ 0.05) in the n-6/n-3 PUFA ratio of liver, kidney and muscle phospholipids relative to vehicle treated controls. Kang Department of Medicine, Massachusetts General Hospital/ Harvard Medical School, Boston, MA 02129, USA Ma (&) Department of Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON N1G 2W1, Canada e-mail: J. Tam-Cre/iFat1 double hybrids were transiently treated with tamoxifen at 6–7 weeks, then terminated 3 weeks later. For in vivo analysis, iFat1 transgenic mice were crossed with the R26-Cre-ERT2 (Tam-Cre) mouse line, a tamoxifen inducible Cre-expression model.
In the presence of Cre, the iFat1 transgene resulted in a balancing (p \ 0.01) of the n-6/n-3 PUFA ratio within phospholipids in the human embryonic kidney 293T cell line. Functionality of the iFat1 transgene was screened both in vitro and in vivo. The aim of this study was to characterize the utility of the iFat1 transgene as a model of Cre-inducible endogenous n-3 PUFA enrichment. To add such capability, the novel Crerecombinase inducible fat-1 (iFat1) transgenic mouse has been developed. This article is published with open access at Ībstract Fat-1 transgenic mice, which endogenously convert n-6 PUFA to n-3 PUFA, are a useful tool in health research however with this model timing of n-3 PUFA enrichment cannot be directly controlled. Received: 25 November 2013 / Accepted: 3 March 2014 / Published online: 13 March 2014 Ó The Author(s) 2014. The iFat1 transgene permits conditional endogenous n-3 PUFA enrichment both in vitro and in vivo Shannon E.
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