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下丘脑多唾液酸化诱导能力的缺乏与适应不良的饮食行为及肥胖易感性相关。

Lack of Hypothalamus Polysialylation Inducibility Correlates With Maladaptive Eating Behaviors and Predisposition to Obesity.

作者信息

Brenachot Xavier, Nédélec Emmanuelle, Ben Fradj Selma, Boudry Gaelle, Douard Véronique, Laderrière Amélie, Lemoine Aleth, Liénard Fabienne, Nuzzaci Danaé, Pénicaud Luc, Rigault Caroline, Benani Alexandre

机构信息

Centre des Sciences du Goût et de l'Alimentation, AgroSup Dijon, CNRS, INRA, Université de Bourgogne, Dijon, France.

Institut NuMeCan, INRA, INSERM, Université Rennes, Domaine de la Prise, Saint-Gilles, France.

出版信息

Front Nutr. 2018 Dec 10;5:125. doi: 10.3389/fnut.2018.00125. eCollection 2018.

Abstract

High variability exists in individual susceptibility to develop overweight in an obesogenic environment and the biological underpinnings of this heterogeneity are poorly understood. In this brief report, we show in mice that the vulnerability to diet-induced obesity is associated with low level of polysialic acid-neural cell adhesion molecule (PSA-NCAM), a factor of neural plasticity, in the hypothalamus. As we previously shown that reduction of hypothalamic PSA-NCAM is sufficient to alter energy homeostasis and promote fat storage under hypercaloric pressure, inter-individual variability in hypothalamic PSA-NCAM might account for the vulnerability to diet-induced obesity. These data support the concept that reduced plasticity in brain circuits that control appetite, metabolism and body weight confers risk for eating disorders and obesity.

摘要

在致肥胖环境中,个体发生超重的易感性存在很大差异,而这种异质性的生物学基础却知之甚少。在本简要报告中,我们在小鼠身上发现,对饮食诱导型肥胖的易感性与下丘脑多唾液酸神经细胞黏附分子(PSA-NCAM,一种神经可塑性因子)水平较低有关。正如我们之前所表明的,下丘脑PSA-NCAM的减少足以改变能量平衡,并在高热量压力下促进脂肪储存,下丘脑PSA-NCAM的个体间差异可能是饮食诱导型肥胖易感性的原因。这些数据支持了这样一种概念,即控制食欲、新陈代谢和体重的脑回路可塑性降低会增加饮食失调和肥胖的风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/162f/6295648/df09843272cd/fnut-05-00125-g0001.jpg

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