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.
Highlights
The endocannabinoid system is deeply involved in the regulation of the homeostasis of body composition by regulating food intake and energy expenditure
[8], we have shown that in Zucker rats, an animal model of obesity, both krill oil (KO) and fish oil increased EPA and DHA plasma levels, with KO being more effective than fish oil in improving some parameters of metabolic syndrome such as fatty liver and fatty heart
Plasma an increase of anandamide (AEA) levels were significantly higher in obese subjects, whereas plasma 2-AG levels were significantly higher only in overweight subjects
Summary
The endocannabinoid system is deeply involved in the regulation of the homeostasis of body composition by regulating food intake and energy expenditure. An overactive endocannabinoid system was suggested to contribute to increased fat mass and to several features of metabolic syndrome [1]. A therapeutic approach aimed at re-establishing a physiological tone of the endocannabinoid system mainly relies on using antagonists of the one of their targets that is mostly responsible for their metabolic effects, i.e. the cannabinoid CB1 receptor [5]. It has been shown that the use of these antagonists in obese individuals is accompanied by psychiatric side effects such as increased incidence of depression and anxiety [5,6]. Endocannabinoids are derived from arachidonic acid incorporated in the sn-1 or sn-2 position of phospholipids, and their biosynthesis was shown to be affected by dietary fatty acids and in particular by EPA and DHA [7]
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