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

Lipids in Health and Disease

Research

Ben Nie¹  Rajesh Amin²  Robert D. Arnold²  Yueru Li³  Chen Zheng³  Guang Ren³  Yinghui Rong³  Lisui Bao³  Ramesh B. Jeganathan⁴  Kevin W. Huggins⁴ 

[1] Department of Drug Discovery and Development, Harrison School of Pharmacy, Auburn University, Auburn, AL, USA;Department of Drug Discovery and Development, Harrison School of Pharmacy, Auburn University, Auburn, AL, USA;Boshell Diabetes and Metabolic Diseases Research Program, Auburn University, Auburn, AL, USA;Department of Nutrition, Dietetics and Hospitality Management, Auburn University, Auburn, AL, USA;Department of Nutrition, Dietetics and Hospitality Management, Auburn University, Auburn, AL, USA;Boshell Diabetes and Metabolic Diseases Research Program, Auburn University, Auburn, AL, USA;

关键词: Obesity;    Stearidonic acid;    Omega-3 fatty acids;    3T3-L1;    Adipocyte differentiation;   

DOI  :  10.1186/s12944-017-0574-7

 received in 2017-06-16, accepted in 2017-09-20,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundIncreased 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.Methods3T3-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).Results3T3-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.ConclusionThese 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.

【 授权许可】

CC BY   
© The Author(s). 2017