Dietary Calanus oil antagonizes angiotensin II-induced hypertension and tissue wasting in diet-induced obese mice.

BACKGROUND: We have recently shown that Calanus oil, which is extracted from the marine copepod Calanus finmarchicus, reduces fat deposition, suppresses adipose tissue inflammation and improves insulin sensitivity in high fat-fed rodents. This study expands upon our previous observations by examining whether dietary supplementation with Calanus oil could antagonize angiotensin II (Ang II)-induced hypertension and ventricular remodeling in mice given a high fat diet (HFD). METHODS: C57BL/6J mice were initially subjected to 8 weeks of HFD with or without 2% (w/w) Calanus oil. Thereafter, animals within each group were randomized for the administration of either Ang II (1µg/kg/min) or saline for another two weeks, while still on the same dietary regimen. RESULTS: Ang II caused a marked decline in body and organ weights in mice receiving non-supplemented HFD, a response which was clearly attenuated in mice receiving Calanus oil supplementation. Furthermore, Ang II-induced elevation in blood pressure was also attenuated in the Calanus oil-supplemented group. As expected, infusion of Ang II produced hypertrophy and up-regulation of marker genes (mRNA level) of both hypertrophy and fibrosis in cardiac muscle, but this response was unaffected by dietary Calanus oil. Fibrosis and inflammation were up-regulated also in the aorta following Ang II infusion. However, the inflammatory response was blocked by Calanus oil supplementation. A final, and unexpected, finding was that dietary intake of Calanus oil caused a robust increase in the level of O-GlcNAcylation in cardiac tissue. CONCLUSION: These results suggest that dietary intake of oil from the marine copepod Calanus finmarchicus could be a beneficial addition to conventional hypertension treatment. The compound attenuates inflammation and the severe metabolic stress caused by Ang II infusion. Although the present study suggests that the anti-hypertensive effect of the oil (or its n-3 PUFAs constituents) is related to its anti-inflammatory action in the vessel wall, other mechanisms such as interaction with intracellular calcium mechanisms or a direct antagonistic effect on Ang II receptors should be examined.

Wax esters from the marine copepod Calanus finmarchicus reduce diet-induced obesity and obesity-related metabolic disorders in mice.

We showed previously 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). After 7 wk, the diet was supplemented with either 1% (wt:wt) WE or 0.2% (wt:wt) E/D. The amount of EPA + DHA in the E/D diet was matched to the total amount of n-3 (ω-3) polyunsaturated fatty acids (PUFAs) in the WE diet. A third group was given an unsupplemented HFD throughout the entire 27-wk feeding period. WE reduced body weight gain, abdominal fat, and liver triacylglycerol by 21%, 34%, and 52%, respectively, and significantly improved glucose tolerance and aerobic capacity. In abdominal fat depots, WE reduced macrophage infiltration by 74% and downregulated expression of proinflammatory genes (tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1), whereas adiponectin expression was significantly upregulated. By comparison, E/D primarily suppressed the expression of proinflammatory genes but had less influence on glucose tolerance than WE. E/D affected obesity parameters, aerobic capacity, or adiponectin expression by <10%. These results show that the wax ester component of Calanus oil can account for the biologic effects shown previously for the crude oil. However, these effects cannot exclusively be ascribed to the content of n-3 PUFAs in the wax ester fraction.

Oil from the marine zooplankton Calanus finmarchicus improves the cardiometabolic phenotype of diet-induced obese mice.

The aim of the present study was to investigate the effects of oil extracted from the zooplankton Calanus finmarchicus (Calanus oil) on diet-induced obesity and obesity-related disorders in mice. C57BL/6J mice fed a high-fat diet (HFD, 45% energy from fat) exhibited increased body weight and abdominal fat accumulation as well as impaired glucose tolerance compared with mice fed a normal chow diet (10% energy from fat). Supplementing the HFD with 1.5% (w/w) Calanus oil reduced body-weight gain, abdominal fat accumulation and hepatic steatosis by 16, 27 and 41%, respectively, and improved glucose tolerance by 16%. Calanus oil supplementation reduced adipocyte size and increased the mRNA expression of adiponectin in adipose tissue. It also reduced macrophage infiltration by more than 70%, accompanied by reduced mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6 and monocyte chemotactic protein-1). The effects of Calanus oil were not only preventive, but also therapeutic, as the oil proved to be beneficial, regardless of whether the supplementation was started before or after the onset of obesity and glucose intolerance. Although the present study cannot pinpoint the active component(s) of the oil, there is reason to believe that the n-3 fatty acids EPA and DHA and/or antioxidants are responsible for its beneficial effects. It should be noted that the concentration of n-3 fatty acids in the Calanus oil diet was considerably lower than the concentrations used in similar studies reporting beneficial effects on obesity and obesity-related abnormalities.

Quantitative MAIPA: Comparison of different MAIPA protocols.

INTRODUCTION: In a screening setting, maternal anti-HPA 1a antibody level has been found to be a good prognostic tool to identify newborns at risk for severe NAIT. AIM: Identify the optimal MAIPA protocol for quantitation of anti-HPA 1a antibodies. MATERIALS AND METHODS: Plasma were analysed for anti-HPA 1a antibodies using different monoclonal antibodies, lyophilized or fresh platelets and MAIPA protocols. RESULTS: The anti-HPA 1a antibody level varied significantly when different monoclonal antibodies were used. However, there was a strong correlation between maternal anti-HPA 1a antibody level and platelet count in the newborn. The sensitivity of the assay depended on the adopted MAIPA protocol. CONCLUSION: Consistent tests results are of importance for the clinical impact of the test.