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目的观察运脾与化湿祛痰药物对饮食诱导肥胖(diet-induced obesity,DIO)大鼠肥胖程度及脂肪激素、瘦素抵抗的影响。方法 Wister大鼠120只,10只作为空白对照组,给予基础饲料,其余110只给予高脂高营养饲料17周,按照体重,得到DIO大鼠40只和肥胖抵抗(diet-in duced obesity resistance,DIOR)大鼠10只,将DIO大鼠又分为DIO模型组、西布曲明组、化湿祛痰组、运脾组4组,每组10只,分别以生理盐水(2 mL/d)、西布曲明(每天1.6 mg/kg)、化湿祛痰药物(每天3.2 g/kg)、运脾药物(每天3.2 g/kg)灌胃,空白对照组与DIO-R组每天予生理盐水(2 mL)灌胃。灌胃期间空白对照组予基础饲料,余5组继续高脂饲料。灌胃16周后,测量体重、身长,取腹腔内全部脂肪,测量肥胖程度及脂肪含量。取血测定胰岛素抵抗指数(insulin resistance index,IRI)、血糖、甘油三酯、胆固醇、瘦素、神经肽Y(neuropeptide Y,NPY)、肿瘤坏死因子(TNF-α)、脂联素(adiponectin)。取脂肪匀浆测定瘦素、TNF-α、脂联素、细胞因子转录负调节因子(suppressor of cytokine signaling-3,SOCS-3)等有关脂肪激素和炎症因子。结果与正常大鼠比较,DIO大鼠体重、体重指数、脂肪系数、IRI、血清瘦素、TNF-α、SOCS-3水平均明显升高(P<0.05,P<0.01),血清NPY和脂肪瘦素、脂联素下降(P<0.05);DIO-R大鼠瘦素升高、NPY降低;与DIO组比较,DIO-R组大鼠体重、体重指数、脂肪系数、IRI、血清NPY、TNF-α、SOCS-3均降低(P<0.05,P<0.01),血清脂肪瘦素、脂联素均升高(P<0.05,P<0.01)。经药物干预治疗后,西布曲明组大鼠体重、体重指数、脂肪系数、脂肪匀浆TNF-α明显降低(P<0.05,P<0.01);化湿祛痰组血清TNF-α降低,脂肪瘦素、脂联素升高(P<0.05),虽体重指数、脂肪系数、IRI、血清瘦素和NPY、SOCS-3有下降趋势,但差异无统计学意义(P>0.05);运脾组体重、体重指数、脂肪系数、IRI、TNF-α、SOCS-3、TNF-α均降低(P<0.05,P<0.01);血清和脂肪瘦素、脂联素均升高(P<0.05,P<0.01)。结论西布曲明可以降低体重,降低脂肪组织TNF-α;运脾药物可以抑制高脂饲料诱导的肥胖和胰岛素抵抗(insulin resistance,IR),药效优于化湿祛痰药物,其机制可能与促进脂肪分泌的瘦素脂联素,降低瘦素抵抗,并升高血清中瘦素、脂联素含量等有关。
Objective To observe the effect of spleen and dampness and expectorant on obesity, adiponectin and leptin resistance in diet-induced obesity (DIO) rats. Methods One hundred and twenty Wister rats were used as blank control group, the basal diet was given, and the remaining 110 were given high-fat and high-nutrition diets for 17 weeks. According to body weight, 40 DIO rats were given diet-in duced obesity resistance DIOR) rats were divided into four groups: DIO model group, sibutramine group, dampness expectorant group and spleen transplantation group, with 10 rats in each group. The rats in each group were treated with normal saline (2 mL / d ), Sibutramine (1.6 mg / kg daily), dampness expectorant drug (3.2 g / kg daily) and spleen drug (3.2 g / kg daily) were orally administered to the rats in the blank control group and the DIO-R group Saline (2 mL) was given orally. Gavage during the control group to the basic diet, the remaining 5 groups continue to high-fat diet. After 16 weeks of gavage, body weight, body length, total fat in the abdominal cavity, fatness and fat content were measured. Blood samples were collected for determination of insulin resistance index (IRI), blood glucose, triglycerides, cholesterol, leptin, neuropeptide Y (NPY), tumor necrosis factor (TNF-), adiponectin . Fetal fat, TNF-α, adiponectin, and suppressor of cytokine signaling-3 (SOCS-3) were measured by lipofectin. Results Compared with normal rats, the body weight, body mass index, fat index, IRI, serum leptin, TNF-α and SOCS-3 in DIO rats were significantly increased (P < Leptin and adiponectin in DIO-R group were significantly lower than those in DIO group (P <0.05). Compared with DIO group, body weight, body mass index, (P <0.05, P <0.01). Serum levels of adiponectin and adiponectin increased (P <0.05, P <0.01). The body weight, body mass index, fat coefficient and TNF-α in fat homogenate decreased significantly in the sibutramine group (P <0.05, P <0.01) after treatment with drug intervention. The serum TNF- Adiponectin and adiponectin increased (P <0.05). Although the body mass index, fat coefficient, IRI, serum leptin and NPY and SOCS-3 had a decreasing trend, the difference was not statistically significant Body weight, body mass index, fat coefficient, IRI, TNF-α, SOCS-3 and TNF-α in spleen group were decreased (P < 0.05, P <0.01). Conclusion Sibutramine can reduce body weight and decrease the level of TNF-α in adipose tissue. Spleen-strengthening drugs can inhibit the obesity and insulin resistance (IR) induced by high-fat diet and its efficacy is better than that of dampness and expectorant drugs. Its mechanism may be And promote the secretion of adiponectin leptin, reduce leptin resistance, and increase serum leptin, adiponectin content and so on.