Send to

Choose Destination
J Lipid Res. 2018 Mar;59(3):452-461. doi: 10.1194/jlr.M081091. Epub 2018 Jan 17.

Impact of dietary ω3 polyunsaturated fatty acid supplementation on brown and brite adipocyte function.

Author information

Université Côte d'Azur, CNRS, Inserm, iBV, Nice, France.
Institute for Diabetes and Cancer (IDC), Helmholtz Zentrum, München, Germany.
Center for Nutritional Medicine, Technical University Munich, Freising, Germany.
Université Côte d'Azur, CNRS, Inserm, iBV, Nice, France


The recent characterization of functional brown adipose tissue in adult humans has opened new perspectives for regulation of energy expenditure with respect to obesity and diabetes. Furthermore, dietary recommendations have taken into account the insufficient dietary intake of ω3 PUFAs and the concomitant excessive intake of ω6 PUFA associated with the occurrence of overweight/obesity. We aimed to study whether ω3 PUFAs could play a role in the recruitment and function of energy-dissipating brown/brite adipocytes. We show that ω3 PUFA supplementation has a beneficial effect on the thermogenic function of adipocytes. In vivo, a low dietary ω6:ω3 ratio improved the thermogenic response of brown and white adipose tissues to β3-adrenergic stimulation. This effect was recapitulated in vitro by PUFA treatment of hMADS adipocytes. We pinpointed the ω6-derived eicosanoid prostaglandin (PG)F2α as the molecular origin because the effects were mimicked with a specific PGF2α receptor agonist. PGF2α level in hMADS adipocytes was reduced in response to ω3 PUFA supplementation. The recruitment of thermogenic adipocytes is influenced by the local quantity of individual oxylipins, which is controlled by the ω6:ω3 ratio of available lipids. In human nutrition, energy homeostasis may thus benefit from the implementation of a more balanced dietary ω6:ω3 ratio.


PUFA; UCP1; adipose tissue; oxylipins; prostaglandins

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center