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A leptin-BDNF pathway regulating sympathetic innervation of adipose tissue

机译：调节脂肪组织交感神经的瘦蛋白-BDNF途径

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摘要

The authors show that leptin signalling regulates the plasticity of sympathetic architecture of adipose tissue via a top-down neural pathway that is crucial for energy homeostasis.Mutations in the leptin gene (ob) result in a metabolic disorder that includes severe obesity(1), and defects in thermogenesis(2)and lipolysis(3), both of which are adipose tissue functions regulated by the sympathetic nervous system. However, the basis of these sympathetic-associated abnormalities remains unclear. Furthermore, chronic leptin administration reverses these abnormalities in adipose tissue, but the underlying mechanism remains to be discovered. Here we report thatob/obmice, as well as leptin-resistant diet-induced obese mice, show significant reductions of sympathetic innervation of subcutaneous white and brown adipose tissue. Chronic leptin treatment ofob/obmice restores adipose tissue sympathetic innervation, which in turn is necessary to correct the associated functional defects. The effects of leptin on innervation are mediated via agouti-related peptide and pro-opiomelanocortin neurons in the hypothalamic arcuate nucleus. Deletion of the gene encoding the leptin receptor in either population leads to reduced innervation in fat. These agouti-related peptide and pro-opiomelanocortin neurons act via brain-derived neurotropic factor-expressing neurons in the paraventricular nucleus of the hypothalamus (BDNFPVH). Deletion of BDNF(PVH)blunts the effects of leptin on innervation. These data show that leptin signalling regulates the plasticity of sympathetic architecture of adipose tissue via a top-down neural pathway that is crucial for energy homeostasis.
机译：作者表明，Leptin信号传导通过对能源稳态至关重要的自上而下的神经途径来调节脂肪组织的同情架构的可塑性。瘦素基因（OB）中导致包括严重肥胖（1）的代谢紊乱，在热生成（2）和脂解（3）中的缺陷，两者都是交感神经系统调节的脂肪组织功能。然而，这些交感神经相关异常的基础仍然尚不清楚。此外，慢性瘦蛋白给药逆转脂肪组织中的这些异常，但仍有待发现的潜在机制。在这里，我们报告说，耐含肽饮食诱导的肥胖小鼠，表现出皮下白色和棕色脂肪组织的交感神经支配的显着减少。慢性瘦素治疗OB / OBMICE恢复脂肪组织交感神经内脏，这反过来是必要的，以纠正相关的功能缺陷。 Leptin对支气管的影响通过丘脑弓核中的刺激相关的肽和Pro-Omiomelanocortin神经元介导。在任何群体中编码瘦素受体的基因缺失导致脂肪的含量降低。这些刺毒相关的肽和Pro-Opiomelanocortin神经元通过脑衍生的神经致因子表达神经元在下丘脑（BDNFPVH）的静脉内核中。缺失BDNF（PVH）钝化瘦素对支配的影响。这些数据显示，瘦素信号传导通过对能源稳态至关重要的自上而下的神经途径来调节脂肪组织的交感神经结构的可塑性。

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  • 来源
    《Nature》 |2020年第7818期|839-844|共6页
  • 作者

    Wang Putianqi; Loh Ken H.; Wu Michelle; Morgan Donald A.; Schneeberger Marc; Yu Xiaofei; Chi Jingyi; Kosse Christin; Kim Damian; Rahmouni Kamal; Cohen Paul; Friedman Jeffrey;

  • 作者单位

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Univ Iowa Dept Pharmacol Iowa City IA 52242 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA|Fudan Univ Sch Life Sci State Key Lab Genet Engn Shanghai Peoples R China;

    Rockefeller Univ Lab Mol Metab 1230 York Ave New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

    Univ Iowa Dept Pharmacol Iowa City IA 52242 USA;

    Rockefeller Univ Lab Mol Metab 1230 York Ave New York NY 10021 USA;

    Rockefeller Univ Howard Hughes Med Inst Lab Mol Genet New York NY 10021 USA;

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