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On the origin of eating disorders: altered signaling between gut microbiota, adaptive immunity and the brain melanocortin system regulating feeding behavior.
Current Opinion in Pharmacology ( IF 4.0 ) Pub Date : 2019-08-21 , DOI: 10.1016/j.coph.2019.07.004
Sergueï O Fetissov 1 , Tomas Hökfelt 2
Affiliation  

Research in the field of gut microbiota - brain axis may contribute to clarifying the origin of anorexia nervosa and bulimia, the two principal forms of eating disorders (ED). The initial key findings in ED patients of plasma immunoglobulins (Ig) that react with α-melanocyte-stimulating hormone (α-MSH), a neuropeptide in the brain signaling satiety, have initiated further studies leading to the discovery of the origin of such autoantibodies and to the understanding their possible functional role. An anorexigenic bacterial protein Escherichia coli caseinolytic protease B was recently found to be responsible for the production of α-MSH-cross-reactive autoantibodies and this protein was also detected in human plasma. Another recent study revealed enhanced activation of appetite-regulating the melanocortin type 4 receptor by immune complexes withα-MSH. Taken together, these data serve to build a pathophysiological model of ED presented in this article.

中文翻译:

关于饮食失调的起源:肠道微生物群,适应性免疫和调节进食行为的大脑黑皮质素系统之间的信号改变。

肠道菌群-脑轴领域的研究可能有助于阐明神经性厌食症和贪食症(饮食失调的两种主要形式)的起源。ED患者血浆中的免疫球蛋白(Ig)与刺激大脑饱足感的神经肽α-黑素细胞刺激激素(α-MSH)反应,最初的主要发现已启动了进一步的研究,导致发现了这种自身抗体并了解其可能的功能作用。最近发现,一种厌食性细菌蛋白大肠杆菌酪蛋白分解蛋白酶B负责产生α-MSH交叉反应性自身抗体,并且还在人血浆中检测到该蛋白。另一项最近的研究表明,与α-MSH的免疫复合物可增强食欲调节黑色素皮质素4型受体的活化。
更新日期:2019-08-17
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