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

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


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / adverse effects*
  • Animals
  • Anti-Inflammatory Agents / administration & dosage*
  • Anti-Inflammatory Agents / pharmacology
  • Aorta / drug effects
  • Body Weight / drug effects
  • Copepoda / chemistry
  • Diet, High-Fat
  • Dietary Fats, Unsaturated / administration & dosage*
  • Dietary Fats, Unsaturated / pharmacology
  • Hypertension / chemically induced
  • Hypertension / diet therapy*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Organ Size / drug effects
  • Random Allocation
  • Treatment Outcome


  • Anti-Inflammatory Agents
  • Dietary Fats, Unsaturated
  • Angiotensin II