Studies on mice show that crude oil extracted from the planktonic copepod Calanus finmarchicus is beneficial at preventing diet induced obesity. In particular, mice fed an obesogenic diet were protected from abdominal obesity, hepatic steatosis, inflammation and insulin resistance by the oil. The crude oil from calanus oil contains a number of substances that could account for the beneficial changes. These include the carotenoid antioxidant astaxanthin, phytosterols eicosapentaenoic acid (EPA, C20:5 (n-3)), docosahexaenoic acid (DHA, C22:6 (n-3)) and monounsaturated fatty acids. Studies have shown that the fatty acids EPA and DHA are protective of dietary induced obesity, and may account for the effects of calanus oil. However, unlike many other sources of marine long chain fatty acids, the EPA and DHA in calanus oil are bound to aliphatic long chain monounsaturated alcohols as wax esters. This is in contrast to most sources where the EPA and DHA are present as fatty acids bound to glycerol as triglycerides.
Because of the differences in the fatty acid composition between calanus oil (wax esters) and other EPA and DHA sources (triglycerides), researchers have investigated the effects of the wax esters from calanus oil against purified fish oils containing EPA and DHA in a purified ethyl ester form. Transgenic mice were induced to obesity through dietary manipulation of the fat content of their diets, and following 7 weeks the diets of the mice were supplemented with either 1 % wax esters extracted from the calanus oil or 0.2 % ethyl esterified EPA and DHA, which provided the same amount of actual EPA and DHA to the mice1. After 20 weeks, the wax ester fed mice had a reduction in body weight, abdominal fat and liver triglycerides of 21, 34 and 52 % respectively. The wax ester mice also showed evidence of improved glucose metabolism and increased aerobic capacity. Inflammatory markers and proinflammatory gene expression fell, whereas adiponectin, a signal molecule associated with lower body weights, showed increased gene expression.
In the ethyl ester EPA and DHA group, there were improvements including increased aerobic capacity, increased adiponectin gene expression, and reductions in inflammation. However the effects were not a great or a wide reaching as those experienced by the mice on the wax ester diet. Therefore the wax esters in the calanus oil can account for the effects of the crude calanus oil at protecting from obesity. However the EPA and DHA component cannot account for all of the effects of the wax esters. Therefore there is some reason that the wax esters provide additional benefits above those provided by just the EPA and DHA component. The authors speculated that the benefits of the wax esters might stem from their delayed absorption rates which delivers EPA and DHA to the distal intestine. Other studies have suggested that in the distal intestine, the EPA and DHA may activate G-protein coupled receptors on L cells, and this may release glucagon like peptide-1 (GLP-1) which causes anti-inflammatory and insulin sensitising effects.
Omega 3 (n-3) fatty acids have been shown to increase fatty acid oxidation rates and this explains their ability to reduce adipocyte accumulation. As adipocyte accumulation stimulates an inflammatory response, the reduced proliferation and growth of adipocytes explains the antiinflammatory effects of the omega 3 fatty acids. Omega 3 fats also likely have a direct effect on the production of inflammatory markers through regulation of eicosanoid synthesis. The reduction in inflammation explains the improvements in glucose homeostasis, as the association between inflammation and insulin resistance is well established. In addition, both monounsaturated and polyunsaturated fatty acids (both present in the wax ester fraction of canalus oil) can switch on PPARδ gene expression, which results in a switch from type II to type I fibre types in skeletal muscle fibres, and this may explain the increased oxidation of fatty acids and the increased aerobic capacity of the mice.
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