Send to

Choose Destination
Br J Nutr. 2013 Dec;110(12):2186-93. doi: 10.1017/S0007114513001839. Epub 2013 Jun 17.

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

Author information

Cardiovascular Research Group, Department of Medical Biology, Faculty of Health Sciences, Institute of Medical Biology, University of Tromsø, N-9037 Tromsø, Norway.


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.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Cambridge University Press
Loading ...
Support Center