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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Leptin-mediated changes in hepatic mitochondrial metabolism, structure, and protein levels
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Leptin-mediated changes in hepatic mitochondrial metabolism, structure, and protein levels

机译：瘦素介导的肝线粒体代谢，结构和蛋白质水平的变化

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摘要

Leptin reduces body weight in ob/ob mice by decreasing food intake and increasing energy expenditure; however, the mechanisms by which it does the latter are not known. Here we report that 30% of the weight loss induced by leptin treatment of ob/ob mice is due to changes in energy expenditure. In assessing leptin's effects on specific tissues, we found that hepatic basal metabolic rate was paradoxically decreased 1.7-fold with leptin treatment, which was the result of a 1.6-fold reduction in mitochondrial volume density and altered substrate oxidation kinetics. The altered kinetics were associated with a decrease in protein levels of 2 mitochondrial respiratory chain components-cytochrome c oxidase subunit Vla and cytochrome c oxi-dase subunit IV. In addition to reduced hepatic metabolism, there was reduced long chain fatty acid production and a 2.5-fold increase in hepatic lipid export, both of which explain the reduced steatosis in leptin-treated animals. These data help clarify the role of the liver in leptin-mediated weight loss and define the mechanisms by which leptin alters hepatic metabolism and corrects steatosis.
机译：瘦素通过减少食物摄入量和增加能量消耗来降低ob / ob小鼠的体重；但是，后者的机制尚不清楚。在这里我们报告说瘦蛋白治疗的ob / ob小鼠引起的体重减轻的30％是由于能量消耗的变化。在评估瘦素对特定组织的影响时，我们发现瘦素治疗使肝脏基础代谢率降低了1.7倍，这是线粒体体积密度降低1.6倍并改变了底物氧化动力学的结果。动力学改变与2个线粒体呼吸链成分-细胞色素c氧化酶亚基Vla和细胞色素c氧化酶亚基IV的蛋白质水平降低相关。除了减少肝脏代谢外，还减少了长链脂肪酸的产生，并使肝脏脂质输出增加了2.5倍，这两者都说明瘦素治疗动物的脂肪变性减少。这些数据有助于阐明肝脏在瘦素介导的体重减轻中的作用，并确定瘦素改变肝脏代谢和纠正脂肪变性的机制。

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    Amandeep Singh; Martin Wirtz; Nadeene Parker; Matthew Hogan; John Strahler; George Michailidis; Sarah Schmidt; Antonio Vidal-Puig; Sabrina Diano; Philip Andrews; Martin D. Brand; Jeffrey Friedman;

  • 作者单位

    Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065;

    Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065;

    Dunn Human Nutrition Unit, Medical Research Council, Hills Road, Cambridge CES2 OXY, England;

    Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065;

    Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065;

    Institute of Metabolic Science, Medical Research Laboratories, University of Cambridge, Cambridge CB20QQ, United Kingdom;

    Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06510;

    Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Ml 48109;

    Medical Research Council Dunn Human Nutrition Unit, Hills Road, Cambridge CB2 OXY, United Kingdom;

    Laboratory of Molecular Genetics, The Rockefeller University, New York, NY 10065 Howard Hughes Medical Institute, New York, NY 10065 The Rockefeller University, 1230 York Avenue, New York, NY 10065;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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