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Eicosapentaenoic acid and arachidonic acid differentially regulate adipogenesis, acquisition of a brite phenotype and mitochondrial function in primary human adipocytes
Author(s) -
FleckensteinElsen Manuela,
Dinnies Daniela,
Jelenik Tomas,
Roden Michael,
Romacho Tania,
Eckel Jürgen
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201500892
Subject(s) - adipogenesis , eicosapentaenoic acid , biology , polyunsaturated fatty acid , adipocyte , arachidonic acid , endocrinology , mitochondrion , docosahexaenoic acid , citrate synthase , mitochondrial respiratory chain , adipose tissue , medicine , fatty acid , biochemistry , enzyme
Scope n‐3 and n‐6 PUFAs have several opposing biological effects and influence white adipose tissue (WAT) function. The recent discovery of thermogenic UCP1‐expressing brite adipocytes within WAT raised the question whether n‐3 and n‐6 PUFAs exert differential effects on brite adipocyte formation and mitochondrial function. Methods and results Primary human preadipocytes were treated with n‐3 PUFAs (eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA) or n‐6 PUFA (arachidonic acid, ARA) during differentiation, and adipogenesis, white and brite gene expression markers, mitochondrial content and function were analyzed at day 12 of differentiation. Adipogenesis was equally increased by n‐3 and n‐6 PUFAs. The n‐6 PUFA ARA increased lipid droplet size and expression of the white‐specific marker TCF21 while decreased mitochondrial protein expression and respiratory function. In contrast, EPA increased expression of the brown adipocyte‐related genes UCP1 and CPT1B, and improved mitochondrial function of adipocytes. The opposing effects of EPA and ARA on gene expression and mitochondrial function were also observed in cells treated from day 8 to 12 of adipocyte differentiation. Conclusion EPA promotes brite adipogenesis and improves parameters of mitochondrial function, such as increased expression of CPTB1, citrate synthase activity and higher maximal respiratory capacity, while ARA reduced mitochondrial spare respiratory capacity in vitro.