Polyunsaturated fatty acid regulation of adipocyte FADS1 and FADS2 expression and function

• Published in: Obesity (Silver Spring, Md.) Md.), 2015-04, Vol.23 (4), p.725-728
• Main Authors: Ralston, Jessica C., Matravadia, Sarthak, Gaudio, Nicholas, Holloway, Graham P., Mutch, David M.
• Format: Article
• Language: English
• Subjects: 3T3-L1 Cells; Adipocytes; Adipocytes - metabolism; Animals; Arachidonic Acid - genetics; Biological activity; Docosahexaenoic Acids; Enzymes; Fatty Acid Desaturases - genetics; Fatty Acid Desaturases - metabolism; Fatty acids; Fatty Acids, Unsaturated - genetics; Fatty Acids, Unsaturated - metabolism; Gene expression; Gene Expression Regulation, Enzymologic; Humans; Hypotheses; Lipids; Metabolism; Mice; Polymorphism, Single Nucleotide; Proteins; Rodents
• ISSN: 1930-7381; 1930-739X
• DOI: 10.1002/oby.21035

Objective Polyunsaturated fatty acids (PUFAs) regulate fatty acid desaturase (FADS1, FADS2) expression in the liver; however, it is unknown whether PUFAs regulate FADS in adipocytes. This is important to study considering reports that link altered desaturase activity with adipose tissue PUFA profiles, body weight, and whole‐body glucose homeostasis. Therefore, the present study aimed to determine the direct effects of PUFAs on FADS expression in differentiated 3T3‐L1 adipocytes. Methods Differentiated 3T3‐L1 adipocytes were treated with either α‐linolenic (ALA), linoleic (LA), eicosapentaenoic (EPA), or arachidonic acid (AA). Gene expression, protein abundance, and cellular PUFA content were analyzed by real‐time RT‐PCR, Western blotting, and gas chromatography, respectively. Results Fads1 and Fads2 gene expression was reduced by EPA and AA, but not ALA or LA. Reductions in gene expression were reflected in FADS2 protein levels, but not FADS1. Treating cells with ALA and LA led to significant increases in the cellular content of downstream PUFAs. Neither ALA nor EPA changed docosahexaenoic acid content. Conclusions Differentiated 3T3‐L1 adipocytes have a functional FADS pathway that can be regulated by PUFA. Therefore, this common adipocyte model is suitable to study dietary regulation of the FADS pathway.