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Miglitol protects against age-dependent weight gain in mice: A potential role of increased UCP1 content in brown adipose tissue

机译:米格列醇可防止小鼠年龄依赖性体重增加:棕色脂肪组织中UCP1含量增加的潜在作用

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摘要

Miglitol is an absorbable alpha-glucosidase inhibitor that is used to control post-prandial hyperglycemia. We previously found that miglitol stimulates brown adipose tissue and prevents diet-induced obesity in mice that are fed a high-fat, high-carbohydrate diet. In this study, we examined whether miglitol can also protect against aging-dependent weight gain in mice that are fed a normal chow diet. Male C57B1/6J mice were fed normal chow with or without miglitol (800 ppm) for 12 weeks, starting at 12 weeks of age. Food intake and body weight were monitored. After 12 weeks, adiposity, energy expenditure, and locomotor activities were measured. After sacrifice, weight of the epididymal white adipose tissue and adipocyte size were measured. Finally, Ucpl gene expression and UCP1 protein abundance in brown adipose tissue were quantified by RT-PCR and Western analyses, respectively. Miglitol prevented age-related weight gain without affecting growth of the animals. Miglitol-treated mice showed reduced adiposity and increased oxygen consumption compared to controls, accompanied by higher UCP1 protein abundance in brown adipose tissue. Food intake and locomotor activities were not affected. These results suggest that miglitol can protect against age-dependent weight gain. Elucidating the molecular targets of miglitol in brown adipose tissue and optimizing drug delivery and efficacy may provide new strategies to combat obesity.
机译:米格列醇是一种可吸收的α-葡萄糖苷酶抑制剂,用于控制餐后高血糖。我们以前发现米格列醇可以刺激棕色脂肪组织,并防止高脂,高碳水化合物饮食喂养的小鼠饮食引起的肥胖。在这项研究中,我们检查了米高糖醇是否还可以预防以普通食物喂养的小鼠的衰老依赖性体重增加。从12周龄开始,对雄性C57B1 / 6J小鼠饲喂含或不含米格列醇(800 ppm)的正常食物12周。监测食物摄入和体重。 12周后,测量肥胖,能量消耗和运动能力。处死后,测量附睾白色脂肪组织的重量和脂肪细胞大小。最后,分别通过RT-PCR和Western分析定量Ucpl基因在棕色脂肪组织中的表达和UCP1蛋白的丰度。米格列醇可防止与年龄有关的体重增加,而不会影响动物的生长。与对照组相比,经米格列醇治疗的小鼠显示出肥胖率降低和耗氧量增加,并伴有棕色脂肪组织中较高的UCP1蛋白丰度。食物摄入和运动活动不受影响。这些结果表明米格列醇可以防止年龄依赖性体重增加。阐明褐色脂肪组织中米格列醇的分子靶标并优化药物递送和功效可能提供抗击肥胖的新策略。

著录项

  • 来源
    《Endocrine journal》 |2015年第5期|469-473|共5页
  • 作者单位

    Laboratory of Metabolic Signal, Institute of Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, 371-8512, Japan;

    Laboratory of Metabolic Signal, Institute of Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, 371-8512, Japan;

    Laboratory of Metabolic Signal, Institute of Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, 371-8512, Japan;

    Laboratory of Metabolic Signal, Institute of Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, 3-39-15 Showa-machi, Maebashi, Gunma, 371-8512, Japan;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Alpha glucosidase inhibitor; Obesity; Brown adipose tissue; UCP1; Energy expenditure;

    机译:α葡萄糖苷酶抑制剂;肥胖;褐色脂肪组织;UCP1;能量消耗;
  • 入库时间 2022-08-18 01:32:20

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