Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju, South Korea.
BMC Complement Altern Med. 2012 Apr 3;12:31. doi: 10.1186/1472-6882-12-31.
Obesity is a health hazard that is associated with a number of diseases and metabolic abnormalities, such as type-2 diabetes, hypertension, dyslipidemia, and coronary heart disease. In the current study, we investigated the effects of Citrus aurantium flavonoids (CAF) on the inhibition of adipogenesis and adipocyte differentiation in 3T3-L1 cells.
During adipocyte differentiation, 3T3-L1 cells were treated with 0, 10, and 50 μg/ml CAF, and then the mRNA and protein expression of adipogenesis-related genes was assayed. We examined the effect of CAF on level of phosphorylated Akt in 3T3-L1 cells treated with CAF at various concentrations during adipocyte differentiation.
The insulin-induced expression of C/EBPβ and PPARγ mRNA and protein were significantly down-regulated in a dose-dependent manner following CAF treatment. CAF also dramatically decreased the expression of C/EBPα, which is essential for the acquisition of insulin sensitivity by adipocytes. Moreover, the expression of the aP2 and FAS genes, which are involved in lipid metabolism, decreased dramatically upon treatment with CAF. Interestingly, CAF diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3β (Ser9), which may reduce glucose uptake in response to insulin and lipid accumulation. Furthermore, CAF not only inhibited triglyceride accumulation during adipogenesis but also contributed to the lipolysis of adipocytes.
In the present study, we demonstrate that CAF suppressed adipogenesis in 3T3-L1 adipocytes. Our results indicated that CAF down-regulates the expression of C/EBPβ and subsequently inhibits the activation of PPARγ and C/EBPα. The anti-adipogenic activity of CAF was mediated by the inhibition of Akt activation and GSK3β phosphorylation, which induced the down-regulation of lipid accumulation and lipid metabolizing genes, ultimately inhibiting adipocyte differentiation.
肥胖是一种健康危害，与许多疾病和代谢异常有关，如 2 型糖尿病、高血压、血脂异常和冠心病。在本研究中，我们研究了酸橙黄酮（CAF）对 3T3-L1 细胞脂肪生成和脂肪细胞分化的抑制作用。
在脂肪细胞分化过程中，用 0、10 和 50μg/ml CAF 处理 3T3-L1 细胞，然后检测脂肪生成相关基因的 mRNA 和蛋白表达。我们研究了 CAF 对 3T3-L1 细胞中 Akt 磷酸化水平的影响，3T3-L1 细胞在脂肪细胞分化过程中用不同浓度的 CAF 处理。
胰岛素诱导的 C/EBPβ和 PPARγ mRNA 和蛋白表达呈剂量依赖性显著下调。CAF 还显著降低了 C/EBPα的表达，C/EBPα是脂肪细胞获得胰岛素敏感性所必需的。此外，参与脂质代谢的 aP2 和 FAS 基因的表达在 CAF 处理后显著降低。有趣的是，CAF 减少了 Akt（Ser473）和 GSK3β（Ser9）的胰岛素刺激丝氨酸磷酸化，这可能会降低胰岛素刺激的葡萄糖摄取和脂质积累。此外，CAF 不仅抑制脂肪生成过程中的甘油三酯积累，而且促进脂肪细胞的脂肪分解。
本研究表明，CAF 抑制 3T3-L1 脂肪细胞的脂肪生成。我们的结果表明，CAF 下调 C/EBPβ的表达，从而抑制 PPARγ和 C/EBPα的激活。CAF 的抗脂肪生成活性是通过抑制 Akt 激活和 GSK3β磷酸化介导的，这导致脂质积累和脂质代谢基因的下调，最终抑制脂肪细胞分化。
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