硫化氢对高脂饮食诱导的肥胖小鼠脂肪代谢的调控作用

The regulation of lipid metabolism by H_2S in diet-induced obesity mice

目的探讨给予外源性硫化氢(H2S)对肥胖小鼠脂肪代谢的调控作用。方法将小鼠分为正常对照组、模型组和治疗组。正常对照组(n=10):给予正常小鼠饲料喂养;模型组(n=10):给予高脂饲料喂养12周建立饮食致胖(diet-induced obesity,DIO)模型;治疗组(n=15):同样建立成DIO小鼠并随机分3小组,分别给予25、50和100μmol·kg-1·d-1 NaHS治疗6周,期间继续给予高脂饲料。给药期间动态监测各组小鼠的体质量变化。治疗期满处死小鼠,检测附睾脂肪以及肾周脂肪重量,用自动生化仪和ELISA法分别检测小鼠血清中的游离脂肪酸(non-esterified fatty acid,NEFA)和抵抗素(resistin)脂肪因子水平。结果与正常对照组比较,DIO模型组小鼠造模成功,体质量、附睾脂肪重量与肾周脂肪重量均有明显升高,但小鼠血清中的NEFA和resistin含量没有明显变化;与模型组相比,治疗各组小鼠附睾脂肪重量与肾周脂肪重量均有明显的回落(P<0.05),血清中的NEFA水平也明显降低(P<0.05),resistin含量没有显著变化。结论 H2S可以显著缓解DIO小鼠脂肪的堆积,降低治疗组血清中NEFA的水平,但对resistin脂肪因子无明显调控作用。

Objective To explore the regulation of lipid metabolism by exogenous hydrogen sulfide （H2S） in mice serum. Methods Mice were divided into a normal group （n=10）, a model group （n=10） and three treatment groups （n=15） of NaHS （25, 50 and 100 μmol·kg^-1·d^-1） as exogenous H2S donor. The normal group was given a normal feed. The diet-induced obesity （DIO） model group mice were induced by using high-fat diet for 12 weeks. Treatment groups received different concentrations of NaHS in saline solution by daily intra peritoneal injection for 6 weeks since the 18th week. Finally, at the end of treatment period, we measured the weight of epididymis adipose and perirenal fat after killing mice of treatment groups. Then the content of non-esterified fatty acid （NEFA） was measured by automatic biochemical analyzer and resistin level was measured with ELISA kit in mice serum. Results Compared with the normal group, the body weight, epididymis adipose weight and perirenal fat weight had obvious increase （P〈0.05）, but the levels of NEFA and resistin did not change significantly in model group; Compared with model group mice, the weight of epididymis adipose and perirenal fat and the level of NEFA had significant decrease in mice of treatment groups （P〈0.05）, but the content of resistin had no obvious change. Conclusions Hydrogen sulfide could obviously reduce the fat accumulation of DIO mice and significantly decrease the serum level of NEFA in treatment groups, but its regulation on resistin was not obvious.