Douglass John D, Dorfman Mauricio D, Thaler Joshua P
UW Diabetes Institute and Department of Medicine, University of Washington, 850 Republican St, S248, Box 358055, Seattle, WA, 98109, USA.
Diabetologia. 2017 Feb;60(2):226-236. doi: 10.1007/s00125-016-4181-3. Epub 2016 Dec 16.
Body weight stability requires homeostatic regulation to balance energy intake and energy expenditure. Research on this system and how it is affected by obesity has largely focused on the role of hypothalamic neurons as integrators of information about long-term fuel storage, short-term nutrient availability and metabolic demand. Recent studies have uncovered glial cells as additional contributors to energy balance regulation and obesity pathogenesis. Beginning with early work on leptin signalling in astrocytes, this area of research rapidly emerged after the discovery of hypothalamic inflammation and gliosis in obese rodents and humans. Current studies have revealed the involvement of a wide variety of glial cell types in the modulation of neuronal activity, regulation of hormone and nutrient availability, and participation in the physiological regulation of feeding behaviour. In addition, one glial type, microglia, has recently been implicated in susceptibility to diet-induced obesity. Together, these exciting new findings deepen our understanding of energy homeostasis regulation and raise the possibility of identifying novel mechanisms that contribute to the pathogenesis of obesity.
体重稳定需要体内平衡调节来平衡能量摄入与能量消耗。对该系统及其受肥胖影响方式的研究主要集中在下丘脑神经元作为长期燃料储存、短期营养可利用性和代谢需求信息整合者的作用上。最近的研究发现神经胶质细胞是能量平衡调节和肥胖发病机制的额外促成因素。从早期关于星形胶质细胞中瘦素信号传导的研究开始,在肥胖啮齿动物和人类中发现下丘脑炎症和胶质细胞增生后,这一研究领域迅速兴起。目前的研究表明,多种神经胶质细胞类型参与调节神经元活动、调节激素和营养可利用性以及参与进食行为的生理调节。此外,一种神经胶质细胞类型,即小胶质细胞,最近被认为与饮食诱导的肥胖易感性有关。这些令人兴奋的新发现共同加深了我们对能量稳态调节的理解,并增加了识别导致肥胖发病机制的新机制的可能性。