The purpose of this study was to assess the effects of voluntary wheel running on the expression of leptin mRNA in rats that are either sensitive (OM) or resistant (S5B/Pl) to diet-induced obesity. Male OM and S5B/Pl rats had ad libitum access to standard rodent diet and water. At 3-5 weeks of age, animals of both strains were randomly assigned to either an exercise or sedentary control group. The exercise groups had 24-h access to a running wheel, and they trained for 7 weeks. During weeks 1-4, animals in both OM and S5B/Pl exercise groups progressively increased their running. During weeks 5-7, S5B/Pl exercisers tended to run more than did OM (approximately 60 vs. 45 km/week), but by the end of the study both groups had an equally greater heart weight (mg/g body weight) and planteris citrate synthase activity than their sedentary controls. Oral glucose tolerance tests performed during the last week of training revealed that compared with their appropriate controls, insulin sensitivity was enhanced (P < 0.05) in OM but not in the S5B/Pl wheel-running groups. Inguinal, epididymal, and retroperitoneal fat pads weighed less in the running than in the nonrunning groups of both strains (P < 0.01). Additionally, exercised animals had an increased percentage of smaller cells (40-60 microm; P < 0.05) and a decreased percentage of larger cells (120-160 microm; P < 0.05) in the epididymal fat depot. Epididymal leptin mRNA measured by Northern blot analysis was reduced in the exercise-trained rats of both strains (P < 0.05). Furthermore, serum leptin was reduced in exercise-trained compared with the control animals of both strains. In comparison to S5B/Pl, control OM animals exhibited both a higher expression and higher circulating levels of leptin (P < 0.05). While serum leptin levels were decreased and food intake was increased in the exercise-trained animals of both strains (P < 0.05), the exact relationship between exercise, leptin, and food intake in this rat model of dietary obesity remains to be determined. Nonetheless, these results suggest that the expression and secretion of leptin can be influenced by exercise training and that these changes (i.e., reduced expression and secretion of protein) can occur independently of changes in whole-body insulin sensitivity and susceptibility to diet-induced obesity.

译文

这项研究的目的是评估对饮食诱导的肥胖症敏感(OM)或有抵抗力(S5B / P1)的大鼠中自愿轮转运动对瘦素mRNA表达的影响。雄性OM和S5B / P1大鼠可自由获得标准啮齿动物饮食和水。在3-5周龄时,将两种品系的动物随机分为运动组或久坐对照组。锻炼组可以在24小时内使用跑轮,他们接受了7周的训练。在1-4周中,OM和S5B / P1运动组中的动物逐渐增加其奔跑。在5-7周内,S5B / P1锻炼者的奔跑倾向要比OM多(大约60 vs. 45 km /周),但是到研究结束时,两组的心脏重量(mg / g体重)均相同。和柠檬酸合酶活性比久坐对照者高。在训练的最后一周进行的口服葡萄糖耐量测试显示,与适当的对照组相比,OM组的胰岛素敏感性增强(P <0.05),而S5B / P1滚轮组则没有。两种菌株的腹股沟,附睾和腹膜后脂肪垫的重量均比非跑步组轻(P <0.01)。另外,运动的动物在附睾脂肪贮存库中具有较小百分比的较小细胞(40-60微米; P <0.05),而具有较大百分比的较小细胞(120〜160微米; P <0.05)。通过Northern印迹分析测量的附睾瘦素mRNA在两种品系的运动训练大鼠中均降低(P <0.05)。此外,与两种品系的对照动物相比,在运动训练中血清瘦素降低。与S5B / P1相比,对照OM动物表现出瘦素的更高表达和更高循环水平(P <0.05)。虽然两种品系的运动训练后动物的血清瘦素水平均下降且食物摄入量增加(P <0.05),但在该大鼠饮食肥胖模型中,运动,瘦素和食物摄入量之间的确切关系仍有待确定。尽管如此,这些结果表明,瘦素的表达和分泌会受到运动训练的影响,并且这些变化(即蛋白质的表达和分泌减少)可以独立于全身胰岛素敏感性的变化和对饮食性肥胖症的易感性而发生。 。

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