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目的通过对膳食诱导肥胖大鼠脂肪细胞SOCS-3进行抑制,探讨是否可以恢复瘦素的抗脂肪合成作用。方法采用SOCS-3小发夹RNA(shRNA)慢病毒,感染瘦素抵抗肥胖大鼠成脂诱导分化后的脂肪细胞,检测SOCS-3的抑制效果。再采用50 nmol/L瘦素处理6 h,观察脂肪合成相关基因(PPARγ及aP2)mRNA表达的变化。结果 SOCS-3 shRNA慢病毒可有效抑制脂肪细胞SOCS-3 mRNA的表达,抑制率达50%。50 nmol/L瘦素处理6 h后,感染SOCS-3 shRNA慢病毒组PPARγ及aP2 mRNA的表达显著降低(P<0.01),空白对照组和感染阴性对照病毒组的表达无明显变化(P>0.05)。结论通过抑制膳食诱导肥胖大鼠的脂肪细胞SOCS-3,在一定程度上可以解除脂肪细胞的瘦素抵抗。
OBJECTIVE: To investigate the inhibitory effect of leptin on the anti-lipogenesis by inhibiting the adipose cell SOCS-3 in diet-induced obese rats. Methods SOCS-3 small hairpin RNA (shRNA) lentivirus was used to infect adiponectin induced adipogenesis induced by leptin in obese rats to detect the inhibitory effect of SOCS-3. Then 50 nmol / L leptin was used for 6 h to observe the changes of mRNA expression of adipose-related genes (PPARγ and aP2). Results SOCS-3 shRNA lentivirus could effectively inhibit the expression of SOCS-3 mRNA in adipocytes with the inhibition rate of 50%. After treated with 50 nmol / L leptin for 6 h, the expression of PPARγ and aP2 mRNA in SOCS-3 shRNA lentivirus group was significantly decreased (P <0.01), but there was no significant difference between blank control group and negative control virus group (P> 0.05). Conclusion By inhibiting SOCS-3 of fat cells in diet-induced obese rats, leptin resistance of adipocytes can be relieved to a certain extent.