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Prostaglandins Leukot Essent Fatty Acids. 2016 May;108:13-21. doi: 10.1016/j.plefa.2016.03.006. Epub 2016 Mar 24.

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

Author information

1
Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway.
2
Faculty of Kinesiology, University of Calgary, 3300 University Drive NW, Calgary, Alberta T2N 4N1, Canada.
3
Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, N-9037 Tromsø, Norway. Electronic address: terje.larsen@uit.no.

Abstract

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.

KEYWORDS:

Hypertension; Inflammation; Marine oil; Obesity; Protein O-GlcNAcylation

PMID:
27154360
DOI:
10.1016/j.plefa.2016.03.006
[Indexed for MEDLINE]

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