Eicosapentaenoic Acid Induces mRNA Expression of Peroxisome Proliferator‐Activated Receptor γ

• Published in: Obesity research 2002-06, Vol.10 (6), p.518-525
• Main Authors: Chambrier, Cécile, Bastard, Jean‐Philippe, Rieusset, Jennifer, Chevillotte, Emmanuel, Bonnefont‐Rousselot, Dominique, Therond, Patrice, Hainque, Bernard, Riou, Jean‐Paul, Laville, Martine, Vidal, Hubert
• Format: Article
• Language: English
• Subjects: Adipocytes - chemistry; Aged; Blood Glucose - analysis; Body Mass Index; Dietary Fats - pharmacology; dietary fatty acids; Docosahexaenoic Acids - blood; Eicosapentaenoic Acid - administration & dosage; Eicosapentaenoic Acid - blood; Eicosapentaenoic Acid - pharmacology; Fatty Acids - blood; Fatty Acids - pharmacology; Fatty Acids, Omega-3 - blood; Female; Gene Expression Regulation - drug effects; gene regulation; Humans; Insulin - blood; insulin resistance; Kinetics; Male; Middle Aged; nuclear receptor; Obesity - metabolism; Receptors, Cytoplasmic and Nuclear - genetics; Reverse Transcriptase Polymerase Chain Reaction; reverse‐transcription competitive polymerase chain reaction; RNA, Messenger - analysis; Transcription Factors - genetics
• ISSN: 1071-7323; 1550-8528
• DOI: 10.1038/oby.2002.70

Objective: To verify whether polyunsaturated fatty acids (PUFAs) can regulate the expression of the nuclear receptor peroxisome proliferator‐activated receptor γ (PPARγ) in human adipose tissue. Research Methods and Procedures: The effect of various PUFAS on PPARγ1 and ‐γ2 mRNA expression was investigated in freshly isolated adipocytes prepared from fat samples obtained during surgery. PPARγ mRNA levels were also determined in subcutaneous adipose tissue biopsies of 11 obese women, in the fasting state, to search for in vivo associations between PPARγ expression and plasma PUFA concentrations. PPARγ mRNA levels were determined by reverse‐transcription competitive polymerase chain reaction. Results: Eicosapentaenoic acid (EPA) significantly increased PPARγ1 mRNA levels in isolated adipocytes, without affecting the expression of PPARγ2. The other tested fatty acids (linolenic acid, docosahexaenoic acid and ω‐6 PUFAs) had no effect. The effect of EPA was dependent on the concentration (maximal effect after 6 hours with 50 μM) and was not reproduced by activators of the different members of the PPAR family. In addition, a strong positive correlation was found between plasma EPA concentrations and PPARγ mRNA levels in adipose tissue of obese subjects. Discussion: Our results demonstrate that adipose tissue PPARγ1 mRNA concentration is positively regulated by EPA, suggesting that the composition of dietary lipids may affect PPARγ gene expression in vivo in humans. These data also suggest that an induction of the expression of this nuclear receptor isoform might be involved in the mechanism of action of EPA and in some of its beneficial effects.