Suppression of adipocyte differentiation and lipid accumulation by stearidonic acid (SDA) in 3T3-L1 cells

• Published in: Lipids in health and disease 2017-09, Vol.16 (1), p.181-181, Article 181
• Main Authors: Li, Yueru, Rong, Yinghui, Bao, Lisui, Nie, Ben, Ren, Guang, Zheng, Chen, Amin, Rajesh, Arnold, Robert D, Jeganathan, Ramesh B, Huggins, Kevin W
• Format: Article
• Language: English
• Subjects: 3T3-L1; 3T3-L1 Cells; Adipocyte differentiation; Adipocytes; Adipocytes - cytology; Adipocytes - drug effects; Adipocytes - metabolism; Analysis; Animals; Care and treatment; CCAAT-Enhancer-Binding Protein-beta - antagonists & inhibitors; CCAAT-Enhancer-Binding Protein-beta - genetics; CCAAT-Enhancer-Binding Protein-beta - metabolism; CCAAT-Enhancer-Binding Proteins - antagonists & inhibitors; CCAAT-Enhancer-Binding Proteins - genetics; CCAAT-Enhancer-Binding Proteins - metabolism; Cell Differentiation - drug effects; Cell Survival - drug effects; Desaturase; Development and progression; Down-regulation; Echium; Fatty Acid Synthase, Type I - antagonists & inhibitors; Fatty Acid Synthase, Type I - genetics; Fatty Acid Synthase, Type I - metabolism; Fatty Acid-Binding Proteins - antagonists & inhibitors; Fatty Acid-Binding Proteins - genetics; Fatty Acid-Binding Proteins - metabolism; Fatty acids; Fatty Acids, Omega-3 - pharmacology; Fatty-acid synthase; Fish oils; Gene expression; Gene Expression Regulation - drug effects; Gene regulation; Glucose transporter; Glucose Transporter Type 4 - antagonists & inhibitors; Glucose Transporter Type 4 - genetics; Glucose Transporter Type 4 - metabolism; Lipase; Lipid Metabolism - drug effects; Lipoprotein lipase; Lipoprotein Lipase - antagonists & inhibitors; Lipoprotein Lipase - genetics; Lipoprotein Lipase - metabolism; Liquid chromatography; Mass spectroscopy; Mice; Obesity; Omega 3 fatty acids; Phosphoenolpyruvate Carboxykinase (ATP) - antagonists & inhibitors; Phosphoenolpyruvate Carboxykinase (ATP) - genetics; Phosphoenolpyruvate Carboxykinase (ATP) - metabolism; Polymerase chain reaction; PPAR gamma - antagonists & inhibitors; PPAR gamma - genetics; PPAR gamma - metabolism; Preadipocytes; Rodents; Soybeans; Stearidonic acid; Stearoyl-CoA desaturase; Stearoyl-CoA Desaturase - antagonists & inhibitors; Stearoyl-CoA Desaturase - genetics; Stearoyl-CoA Desaturase - metabolism; Sterol Regulatory Element Binding Protein 1 - antagonists & inhibitors; Sterol Regulatory Element Binding Protein 1 - genetics; Sterol Regulatory Element Binding Protein 1 - metabolism; Sterol regulatory element-binding protein; Toxicity; Transcription factors; Vegetable oils
• ISSN: 1476-511X; 1476-511X
• DOI: 10.1186/s12944-017-0574-7

Increased consumption of omega-3 (ω-3) fatty acids found in cold-water fish and fish oil has been reported to protect against obesity. A potential mechanism may be through reduction in adipocyte differentiation. Stearidonic acid (SDA), a plant-based ω-3 fatty acid, has been targeted as a potential surrogate for fish-based fatty acids; however, its role in adipocyte differentiation is unknown. This study was designed to evaluate the effects of SDA on adipocyte differentiation in 3T3-L1 cells. 3T3-L1 preadipocytes were differentiated in the presence of SDA or vehicle-control. Cell viability assay was conducted to determine potential toxicity of SDA. Lipid accumulation was measured by Oil Red O staining and triglyceride (TG) quantification in differentiated 3T3-L1 adipocytes. Adipocyte differentiation was evaluated by adipogenic transcription factors and lipid accumulation gene expression by quantitative real-time polymerase chain reaction (qRT-PCR). Fatty acid analysis was conducted by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). 3T3-L1 cells treated with SDA were viable at concentrations used for all studies. SDA treatment reduced lipid accumulation in 3T3-L1 adipocytes. This anti-adipogenic effect by SDA was a result of down-regulation of mRNA levels of the adipogenic transcription factors CCAAT/enhancer-binding proteins alpha and beta (C/EBPα, C/EBPβ), peroxisome proliferator-activated receptor gamma (PPARγ), and sterol-regulatory element binding protein-1c (SREBP-1c). SDA treatment resulted in decreased expression of the lipid accumulation genes adipocyte fatty-acid binding protein (AP2), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD-1), lipoprotein lipase (LPL), glucose transporter 4 (GLUT4) and phosphoenolpyruvate carboxykinase (PEPCK). The transcriptional activity of PPARγ was found to be decreased with SDA treatment. SDA treatment led to significant EPA enrichment in 3T3-L1 adipocytes compared to vehicle-control. These results demonstrated that SDA can suppress adipocyte differentiation and lipid accumulation in 3T3-L1 cells through down-regulation of adipogenic transcription factors and genes associated with lipid accumulation. This study suggests the use of SDA as a dietary treatment for obesity.