The sympathetic neuro-adipose connection and the control of body weight.

The sympathetic neuro-adipose connection and the control of body weight.
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DOI:
10.1016/j.yexcr.2017.03.047
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发表时间:
2017-11-01
影响因子:
3.7
通讯作者:
Domingos AI
Domingos AI
中科院分区:
医学3区
文献类型:
--
作者:
Mahú I;Domingos AI

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近几十年来,肥胖已成为一种全球公共健康危机,不分年龄和性别。但根据历史记录,人们对适当保持体型的担忧由来已久。两千多年来,控制超重的主要治疗方法一直是建议限制饮食和定期锻炼。然而,更多的当代研究表明,在严重肥胖患者的治疗中使用这种方法会导致代谢适应,从而损害他们在体重管理方面的长期成功。因此,这些证据突出表明,迫切需要更全面地了解控制体重的机制,这对于制定有效的肥胖症及其并存治疗战略至关重要。重要的是,激素瘦素的发现和靶向转基因新技术的使用使人们在确定一些关键因素和分子机制方面取得了进展,这些因素和分子机制参与了控制身体尺寸动态平衡和能量平衡的过程,以及肥胖可能如何扰乱瘦素的反馈循环并导致代谢综合征的病理。根据这些发现,我们在这里回顾了交感神经系统如何在瘦素对中枢神经系统的作用之后调节脂肪组织的代谢,特别是在过度肥胖的背景下这一系统如何被破坏,并强调了更好地理解交感神经-脂肪连接的生理控制所产生的潜在的临床意义。
In recent decades, obesity has become a global public health crisis irrespective of age or gender. But according to historic records, concerns over appropriate maintenance of body size have been long established. For more than to 2 millennia, the main therapeutic approach to curb excess weight has been to recommend dietary restrictions and regular exercise. Nevertheless, more contemporary studies indicate that the employment of such approaches in the treatment of severely obese patients causes metabolic adaptions which impair their long-term success in weight management. These evidences highlight thus, the urgency in the search for a more comprehensive knowledge of the mechanisms that underlie the control of body weight, which would be essential for the development of effective strategies for the treatment of obesity and its comorbidities. Importantly, the discovery of the hormone leptin and the use of novel techniques in targeted transgenesis have enabled progress in defining some of the key players and the molecular mechanisms that are involved in the processes that control body size homeostasis and energy balance, and how obesity may disrupt leptin’s feedback loop and lead to the pathology of metabolic syndrome. On the light of such findings, here we review how the sympathetic nervous system modulates adipose tissue metabolism downstream of leptin's action on the CNS, with particular focus on how this system may be disrupted in the context of excess adiposity, plus highlight the potential clinical implications arising from a better understanding of the physiologic control of the sympathetic neuro-adipose connection.
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