Mahú Inês, Domingos Ana I
Obesity Laboratory, Instituto Gulbenkian de Ciência, Oeiras, Portugal.
Obesity Laboratory, Instituto Gulbenkian de Ciência, Oeiras, Portugal.
Exp Cell Res. 2017 Nov 1;360(1):27-30. doi: 10.1016/j.yexcr.2017.03.047. Epub 2017 Mar 22.
In recent decades, obesity has become a global public health crisis irrespective of age or gender [20]. 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 (Haslam, 2016). 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 [8]. 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 [33]and the use of novel techniques in targeted transgenesis [32] 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.
近几十年来，肥胖已成为全球性的公共卫生危机，不分年龄或性别[20]。但根据历史记录，对适当维持体型的关注由来已久。两千多年来，控制体重的主要治疗方法一直是建议饮食限制和定期锻炼（哈斯拉姆，2016年）。然而，更多当代研究表明，在治疗严重肥胖患者时采用这些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效[8]。因此，这些证据凸显了迫切需要更全面地了解体重控制背后的机制，这对于制定治疗肥胖及其合并症的有效策略至关重要。重要的是，激素瘦素的发现[33]以及靶向转基因新技术的应用[32]，使得在确定控制体型稳态和能量平衡过程中涉及的一些关键因素和分子机制，以及肥胖如何破坏瘦素的反馈回路并导致代谢综合征病理方面取得了进展。鉴于这些发现，我们在此回顾交感神经系统如何在瘦素作用于中枢神经系统的下游调节脂肪组织代谢，特别关注在肥胖情况下该系统可能如何被破坏，并强调更好地理解交感神经 - 脂肪连接的生理控制所产生的潜在临床意义。
