A comprehensive molecular mechanistic role of lutein on adipogenesis is not well understood. The present study focused to evaluate the effect of lutein at the early and late phase of adipocyte differentiation in vitro using a 3T3-L1 cell model. The effect of purified carotenoid on the viability of normal and differentiated 3T3-L1 cells was analyzed by WST-1 assay. Oil Red O and Nile red staining were employed to observe lipid droplets in mature adipocytes. The effect of lutein on gene and protein expression of major transcription factors and adipogenic markers was analyzed by RT-PCR and western blotting, respectively. The role of lutein on mitotic clonal expansion was analyzed by flow cytometry. The results showed a significant reduction (p < 0.05) in the accumulation of lipid droplets in lutein-treated (5 μM) cells. Inhibition in lipid accumulation was associated with down-regulated expression of CEBP-α and PPAR-γ at gene and protein levels. Subsequently, lutein repressed gene expression of FAS, FABP4, and SCD1 in mature adipocytes. Interestingly, it blocks the protein expression of CEBP-α and PPAR-γ in the initial stages of adipocyte differentiation. This early-stage inhibition of adipocyte differentiation is linked with repressed phosphorylation AKT and ERK. Further, upregulated cyclin D and down-regulated CDK4 and CDK2 in lutein treated adipocytes enumerate its role in delaying the cell cycle progression at the G0/G1 phase. Our results emphasize that adipogenesis inhibitory efficacy of lutein is potentiated by halting early phase regulators of adipocyte differentiation, which strengthens the competency of lutein besides its inevitable presence in the human body.

叶黄素在脂肪形成中的全面分子机制作用尚不清楚。本研究的重点是使用3T3-L1细胞模型评估叶黄素在体外脂肪细胞分化的早期和晚期的作用。用WST-1分析法分析纯化的类胡萝卜素对正常和分化的3T3-L1细胞活力的影响。用油红O和尼罗红染色观察成熟脂肪细胞中的脂质滴。通过RT-PCR和western blotting分析叶黄素对主要转录因子和成脂标记基因和蛋白质表达的影响。通过流式细胞术分析叶黄素在有丝分裂克隆扩增中的作用。结果显示显着降低（p <0.05）在叶黄素处理过的（5μM）细胞中脂质液滴的积累。脂质蓄积的抑制与基因和蛋白质水平上CEBP-α和PPAR-γ的表达下调有关。随后，叶黄素抑制成熟脂肪细胞中FAS，FABP4和SCD1的基因表达。有趣的是，它在脂肪细胞分化的初期阻断了CEBP-α和PPAR-γ的蛋白表达。脂肪细胞分化的这种早期抑制与抑制的AKT和ERK磷酸化有关。此外，叶黄素处理的脂肪细胞中细胞周期蛋白D的上调和CDK4和CDK2的下调列举了其在延迟G0 / G1期细胞周期进程中的作用。我们的结果强调，通过停止脂肪细胞分化的早期调节剂来增强叶黄素的脂肪生成抑制功效，