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目的探讨亮氨酸对高脂高胆固醇喂养小鼠体脂和瘦素抵抗的影响。方法 60只雄性C57BL/6J小鼠随机分为对照组、高脂高胆固醇组、低、高剂量亮氨酸组(1.5%、3.0%亮氨酸),干预24周;测定小鼠体重、脂肪重量、血清胆固醇和瘦素水平,Western blot法检测小鼠睾周脂肪组织中瘦素受体(Ob-R)、Janus蛋白酪氨酸激酶2(JAK2)、信号转导和转录激活子3(STAT3)及细胞因子信号转导抑制因子3(SOCS3)的蛋白表达。结果高脂高胆固醇喂养明显升高小鼠体重、脂重和血清胆固醇水平;与高脂高胆固醇组比较,亮氨酸组小鼠体重、脂重和血清胆固醇水平明显下降;与对照组比较,高脂高胆固醇组小鼠血清瘦素水平明显升高[(7.14±2.44)ng/mL,](P<0.01);与高脂高胆固醇组比较,1.5%、3.0%亮氨酸组小鼠瘦素水平[分别为(4.21±2.37)、(4.24±2.22)ng/mL]明显降低(P<0.01);与对照组比较,高脂高胆固醇组小鼠睾周脂肪组织中Ob-R蛋白表达下调;与高脂高胆固醇组比较,亮氨酸组小鼠睾周脂肪组织中Ob-R、JAK2蛋白表达上调、SOCS3蛋白表达下调。结论亮氨酸干预可抑制高脂高胆固醇喂养引起的小鼠体重和体脂增加,其机制可能与调节瘦素受体及其下游蛋白JAK2和SOCS3表达、改善瘦素抵抗有关。
Objective To investigate the effect of leucine on body fat and leptin resistance in high fat and cholesterol fed mice. Methods Sixty male C57BL / 6J mice were randomly divided into control group, high fat and high cholesterol group, low and high dose leucine group (1.5%, 3.0% leucine) for 24 weeks. The body weight, (OB-R), Janus protein tyrosine kinase 2 (JAK2), signal transducers and activators of transcription 3 ( STAT3) and cytokine signal transduction inhibitor 3 (SOCS3) protein expression. Results High-fat and high-cholesterol diet significantly increased body weight, lipid and serum cholesterol in mice. Compared with high-fat and high-cholesterol group, body weight, lipid and serum cholesterol in leucine group decreased significantly. Compared with control group, Serum leptin level was significantly increased in high fat and high cholesterol group [(7.14 ± 2.44) ng / mL, P <0.01). Compared with high fat and high cholesterol group, 1.5% and 3.0% leucine groups (4.21 ± 2.37, 4.24 ± 2.22 ng / mL, respectively) (P <0.01). Compared with the control group, the levels of Ob-R protein in the testicular adipose tissue of high-fat and high-cholesterol group The expression of Ob-R and JAK2 in the leucocytes of leucine group was up-regulated and the expression of SOCS3 protein was down-regulated. Conclusion Leucine can inhibit the increase of body weight and body fat in mice induced by high-fat and high-cholesterol diet. The mechanism may be related to the regulation of leptin receptor and its downstream proteins JAK2 and SOCS3, and the improvement of leptin resistance.