Open Access Research

Krill oil significantly decreases 2-arachidonoylglycerol plasma levels in obese subjects

Sebastiano Banni12*, Gianfranca Carta12, Elisabetta Murru12, Lina Cordeddu12, Elena Giordano12, Anna Rita Sirigu12, Kjetil Berge3, Hogne Vik3, Kevin C Maki4, Vincenzo Di Marzo5 and Mikko Griinari6

Author Affiliations

1 Dipartimento Biologia Sperimentale, Università di Cagliari, Cittadella Universitaria, 09042 Monserrato (CA), Italy

2 Nutrisearch s.r.l., Edificio 5 A1 Parco scientifico e tecnologico Polaris,09010 Pula, Italy

3 Aker Biomarine ASA, Fjordallèen 16, NO-0115 Oslo, Norway

4 Provident Clinical Research, 489 Taft Avenue, Glen Ellyn, Illinois 60137, USA

5 Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, Comprensorio Olivetti, 80078 Pozzuoli (NA), Italy

6 Clanet Ltd., Kultarinnantie 1 b, Espoo, 02660, Finland

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Nutrition & Metabolism 2011, 8:7  doi:10.1186/1743-7075-8-7

Published: 30 January 2011

Abstract

We have previously shown that krill oil (KO), more efficiently than fish oil, was able to downregulate the endocannabinoid system in different tissues of obese zucker rats.

We therefore aimed at investigating whether an intake of 2 g/d of either KO or menhaden oil (MO), which provides 309 mg/d of EPA/DHA 2:1 and 390 mg/d of EPA/DHA 1:1 respectively, or olive oil (OO) for four weeks, is able to modify plasma endocannabinoids in overweight and obese subjects.

The results confirmed data in the literature describing increased levels of endocannabinoids in overweight and obese with respect to normo-weight subjects. KO, but not MO or OO, was able to significantly decrease 2-arachidonoylglycerol (2-AG), although only in obese subjects. In addition, the decrease of 2-AG was correlated to the plasma n-6/n-3 phospholipid long chain polyunsaturated fatty acid (LCPUFA) ratio. These data show for the first time in humans that relatively low doses of LCPUFA n-3 as KO can significantly decrease plasma 2-AG levels in obese subjects in relation to decrease of plasma phospholipid n-6/n-3 LCPUFA ratio. This effect is not linked to changes of metabolic syndrome parameters but is most likely due to a decrease of 2-AG biosynthesis caused by the replacement of 2-AG ultimate precursor, arachidonic acid, with n-3 PUFAs, as previously described in obese Zucker rats.