Lebrun Bruno, Bariohay Bruno, Moyse Emmanuel, Jean André
Laboratoire de Physiologie Neurovégétative (PNV), UMR Université Paul Cézanne Aix, Marseille III, CNRS (UMR 6153), INRA (UMR 1147), Faculté des sciences et techniques, BP 351, 13397 Marseille cedex 20, France.
Auton Neurosci. 2006 Jun 30;126-127:30-8. doi: 10.1016/j.autneu.2006.02.027. Epub 2006 Apr 24.
Neurotrophins, and in particular BDNF, play important roles in proliferation, differentiation and survival of neurons during development, as well as in the synaptic activity and plasticity in many groups of mature neurons. Several lines of evidence suggest that BDNF and its high affinity receptor TrkB contribute to food intake and body weight control. In rodents, pharmacological treatments with BDNF induce reduction in food intake, whereas genetic models with an altered BDNF/TrkB signalling display hyperphagia and obesity. Genetic studies in humans have shown that mutations in the BDNF or TrkB genes may account for certain types of obesity or other forms of eating disorders. Since circulating levels of BDNF correlate with eating disorders in humans and peripheral BDNF treatments reduce hyperphagia and hyperglycaemia in obese diabetic rodents, an endocrine role of BDNF appears plausible and requires further investigation. A central anorectic action of BDNF has also been documented, with a primary focus on the hypothalamus and a more recent highlight on the brainstem integrator of energy homeostasis, the dorsal vagal complex. In this review, we will briefly present neurotrophins and their receptors and focus on experimental evidence which point out BDNF as a signalling component of food intake regulation, with a particular emphasis on the localization of the central anorectic action of BDNF.
神经营养因子，尤其是脑源性神经营养因子（BDNF），在神经元发育过程中的增殖、分化和存活中发挥着重要作用，同时也在许多成熟神经元群体的突触活动和可塑性中发挥作用。多项证据表明，BDNF及其高亲和力受体TrkB参与食物摄入和体重控制。在啮齿动物中，BDNF的药物治疗会导致食物摄入量减少，而BDNF/TrkB信号改变的遗传模型则表现出食欲亢进和肥胖。人类的遗传学研究表明，BDNF或TrkB基因的突变可能是某些类型肥胖或其他形式饮食失调的原因。由于人类循环中的BDNF水平与饮食失调相关，并且外周给予BDNF治疗可减少肥胖糖尿病啮齿动物的食欲亢进和高血糖，因此BDNF的内分泌作用似乎合理，需要进一步研究。BDNF的中枢性厌食作用也有文献记载，主要集中在下丘脑，最近则聚焦于能量稳态的脑干整合器——迷走背核复合体。在这篇综述中，我们将简要介绍神经营养因子及其受体，并重点关注指出BDNF作为食物摄入调节信号成分的实验证据，特别强调BDNF中枢性厌食作用的定位。
