Effect of Astaxanthin on the Inhibition of Lipid Accumulation in 3T3-L1 Adipocytes via Modulation of Lipogenesis and Fatty Acid Transport Pathways

• Published in: Molecules (Basel, Switzerland) Vol. 25; no. 16; p. 3598
• Main Authors: Tsai, Mei-Chih, Huang, Shih-Chien, Chang, Wei-Tang, Chen, Shiuan-Chih, Hsu, Chin-Lin
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 07.08.2020; MDPI
• Subjects: 3T3-L1 adipocytes; 3T3-L1 Cells; Adipocytes; Adipocytes - cytology; Adipocytes - drug effects; Adipocytes - metabolism; Adipogenesis - drug effects; Animals; Antioxidants; astaxanthin; Biological Transport - drug effects; Cardiovascular disease; Carotenoids; Enzymes; Fatty acids; Fatty Acids - metabolism; Gene expression; Glycerol; Intracellular Space - drug effects; Intracellular Space - metabolism; Lipids; lipogenesis; Lipogenesis - drug effects; Lipoproteins; Metabolism; Mice; Obesity; Oxidative stress; Proteins; Triglycerides - metabolism; Xanthophylls - pharmacology; 3T3-L1 adipocytes; lipogenesis; gene expression; astaxanthin
• DOI: 10.3390/molecules25163598
• ISSN: 1420-3049

Obesity is defined as a condition of excessive fat tissue accumulation. It was the major factor most closely associated with lifestyle-related diseases. In the present study, we investigated the effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated with 0–25 µg/mL of astaxanthin for 0–48 h. The result indicated that astaxanthin significantly decreased the oil Red O stained material (OROSM), intracellular triglyceride accumulation, and glycerol 3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes (p < 0.05). At the molecular level, astaxanthin significantly down-regulated the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) in 3T3-L1 adipocytes (p < 0.05). Moreover, target genes of PPARγ on the inhibition of lipogenesis, such as Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), fatty acid binding protein (aP2), cluster of differentiation 36 (CD36), and lipoprotein lipase (LPL) in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner (p < 0.05). These results suggested that astaxanthin efficiently suppressed lipid accumulation in 3T3-L1 adipocytes and its action is associated with the down-regulation of lipogenesis-related genes and the triglyceride accumulation in 3T3-L1 adipocytes. Therefore, astaxanthin can be developed as a potential nutraceutical ingredient for the prevention of obesity in a niche market.