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The Formation of Diradylglycerol Molecular Species in Murine Peritoneal Macrophages Varies Dose-Dependently with Dietary Purified Eicosapentaenoic and Docosahexaenoic Ethyl Esters^1,2,

Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada L8N 3Z5

Substantial effects of dietary fish oil-derived fatty acid ethyl esters on the metabolism of diradylglycerol (DG) have recently been described. We undertook to isolate the separate effects of (n-3) eicosapentaenoic acid (EPA) and (n-3) docosahexaenoic acid (DHA) on DG metabolism. For 3 wk, male C57BL/6 mice were fed one of six purified diets in which the lipid component was either 3 g/100 g corn oil ethyl ester (COEE) (control diet) or 1 g/100 g COEE plus 2 g/100 g of EPA ethyl ester (EPEE), DHA ethyl ester (DHEE) or an EPEE:DHEE mixture. Peritoneal macrophages were analyzed for DG content and for molecular species distributions of DG and phospholipid classes. We found that the degree of incorporation of EPA and DHA into DG in macrophages was dependent on the dietary concentration of EPEE and DHEE, under basal conditions and after stimulation with platelet-activating factor, phorbol myristate acetate and ionomycin. Incorporation of EPA and DHA into phospholipids was also significant and dose dependent in each phospholipid class. For both DG and phospholipid molecular species, the incorporation of EPA in the sn-2 position was considerably greater than that of species with DHA under conditions of equimolar dietary content. These results demonstrate that 1) incorporation of EPA and DHA into DG are independent and dependent on dietary content, 2) EPA is incorporated with greater affinity than DHA and 3) these effects on DG metabolism seem to result from corresponding effects on parent membrane phospholipids. Physiologically and therapeutically relevant differences may exist between EPA and DHA.

KEY WORDS: • diradylglycerol molecular species • mice • peritoneal macrophages • eicosapentaenoic ethyl ester • docosahexaenoic ethyl ester

¹ Supported by grants from the Arthritis Society of Canada. RJS is the recipient of a Career Award from the Pharmaceutical Manufacturers' Association of Canada-Health Research Foundation and the Medical Research Council of Canada. PAM is the recipient of a Graduate Research Studentship from the Pharmaceutical Manufacturers' Association of Canada-Health Research Foundation and the Medical Research Council of Canada.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence and reprint requests should be addressed.

Manuscript received 22 February 1996. Revision accepted 29 July 1996.

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