Summary of the Scientific Study:
Research study reported that dietary supplementation with oil from the marine zooplankton Calanus finmarchicus (Calanus oil) attenuates obesity, inflammation, and glucose intolerance in mice. More than 80% of Calanus oil consists of wax esters, i.e., long-chain fatty alcohols linked to long-chain fatty acids. In the present study, we compared the metabolic effects of Calanus oil-derived wax esters (WE) with those of purified eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) ethyl esters (E/D) in a mouse model of diet-induced obesity. C57BL/6J mice received a high-fat diet (HFD; 45% energy from fat).
The scientists reported recently that dietary supplementation with oil from the marine zooplankton C. finmarchicus reduces diet-induced obesity and attenuates obesity-related metabolic disorders in mice (3). The biochemical composition of this oil is notably different from that of other marine oils, containing ~80% wax esters, i.e., aliphatic long-chain fatty alcohols esterified to saturated or unsaturated FAs. In the present study, we show that dietary supplementation with the Calanus oil-derived wax ester (WE) exerts similar effects as the crude oil. When compared with E/D, the former showed a superior effect.
Beneficial health effects of marine oils have traditionally been ascribed to their content of n–3 PUFAs, particularly EPA and DHA, and many studies have shown that n–3 PUFAs can counteract obesity-related metabolic disturbances (5,10–13). The present study on diet-induced obese mice demonstrated that supplementation of the diet with WE reduced body weight and abdominal (perirenal) fat stores. WE supplementation also re- duced plasma free FAs and hepatic steatosis and improved glu- cose homeostasis and aerobic capacity in this model. It is important to emphasize that the amount of n–3 PUFAs in the WE-supplemented diet was markedly lower than that of diets used in previous studies with marine oils in rodents, in which anti-obesity and insulin-sensitizing effects were reported (5,12,13). Of particular note, when the diet was supplemented with an equally low amount of E/D, we did not observe a clear anti-obesity effect, in neither the form of body weight reduction nor reductions of abdominal fat mass or hepatic TAG content. WE was also superior to E/D with regard to improvements in glucose tolerance and stimulation of adiponectin expression in adipose tissue.
In line with the well-established link between low-grade inflammation in adipose tissue and insulin resistance (29,30), the present study showed that the reduced inflammatory state after WE supplementation was accompanied by reduced circulating glucose and insulin concentrations, as well as improved glucose tolerance. The inflammatory state was also reduced in mice receiving E/D-supplemented diet, whereas plasma glucose, glucose tolerance, and insulin values were only modestly affected. The explanation for this finding is not clear, but the markedly lower expression of the insulin-sensitizing hormone adiponectin in adipose tissue of the E/D group might be one explanatory factor. However, the etiology of insulin resistance is multifactorial (31), and several studies have reported a positive correlation between liver fat and insulin resistance/glucose dysregulation (32–34). In contrast to WE treatment, hepatic steatosis was not reduced in response to E/D, which could be another factor explaining their less pronounced effect on glucose homeostasis.
Although mammals are considered to use wax esters to only a small extent (35), intestinal uptake of WE or of their hydrolytic products are reported in rats, mice, and dogs (36–40). Also, Gorreta et al. (39) reported similar bioavailability of n–3 PUFAs in rodents, regardless of whether the FAs were given in the form of TAG, ethyl ester, or wax ester. However, delayed digestion of wax esters has been proposed, suggesting that hydrolysis and liberation of biologically active components occurs primarily in the distal part of the intestine (41). Interestingly, Morishita et al. (42) showed that secretion of glucagon-like peptide-1 and the decline of plasma glucose after a glucose load were increased when DHA and EPA was delivered locally in the colon but not in the stomach or proximal jejunum. Glucagon-like peptide-1– producing L-cells have been localized in the distal intestine (ileum and colon), in which they are colocated with the n–3 PUFA G-protein–coupled receptor 120 (GPR120) (43). GPR 120 has been shown recently to mediate potent anti-inflammatory and insulin-sensitizing actions (11,44).
Therefore, it is tempting to speculate that the beneficial metabolic effects of WE observed in the present study could (at least in part) be explained in terms of intestinal GPR 120 activation attributable to delayed WE digestion.
Collectively, the data from the present study show that Calanus oil-derived wax esters (WE) are superior to the ethyl esters of purified EPA + DHA. The biochemical differences of the 2 preparations, in terms of either esterification to an ethyl group (E/D) vs. a long-chain fatty alcohol (WE) or their different FA composition could possibly account for the observed differences between these 2 groups.
Höper, A.C., Salma, W., Sollie, S.J., Hafstad, A.D., Lund, J., Khalid, J., Raa, J., Aasum, E. & Larsen,T.S. (2014). Wax Esters from the Marine Copepod Calanus finmarchicus Reduce Diet-Induced Obesity and Obesity-Related Metabolic Disorders in Mice. Journal of Nutrition, 144 (2): 164-169