| Summary: | 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 (<i>p</i> < 0.05). At the molecular level, astaxanthin significantly down-regulated the mRNA expression of <i>peroxisome proliferator-activated receptor-γ</i> (<i>PPARγ</i>) in 3T3-L1 adipocytes (<i>p</i> < 0.05). Moreover, target genes of <i>PPARγ</i> on the inhibition of lipogenesis, such as <i>Acetyl-CoA carboxylase</i> (<i>ACC</i>), <i>fatty acid synthase</i> (<i>FAS</i>), <i>fatty acid binding protein</i> (<i>aP2</i>), <i>cluster of differentiation 36</i> (<i>CD36</i>), and <i>lipoprotein lipase</i> (<i>LPL</i>) in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner (<i>p</i> < 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.
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