Dataset related to the article-BDNF Val66Met polymorphism alters food intake and hypothalamic BDNF expression in mice

This record contains raw data related to the article "BDNF Val66Met polymorphism alters food intake and hypothalamic BDNF expression in mice" Abstract Obesity, a rising public health burden, is a multifactorial disease with an increased risk for patients to develop several pathological conditions including type 2 diabetes mellitus, hypertension, and cardiovascular disease. Increasing evidence suggests a relationship between the human brain‐derived neurotrophic factor (BDNF) Val66Met single‐nucleotide polymorphism (SNP) and obesity, although the underlying mechanisms of this connection are still not completely understood. In the present study, we found that homozygous knock‐in BDNFMet/Met mice were overweight and hyperphagic compared to wildtype BDNFVal/Val mice. Increased food intake was associated with reduction of total BDNF and BDNF1, BDNF4 and BDNF6 transcripts in the hypothalamus of BDNFMet/Met mice. In contrast, in the white adipose tissue total BDNF and Glut4 expression levels were augmented, while sirtuin 1 and leptin receptor (Ob‐R) expression levels were reduced in BDNFMet/Met mice. Moreover, plasmatic leptin levels were decreased in BDNFMet/Met mice. However, BDNFVal/Val and BDNFMet/Met mice showed a similar response to the insulin tolerance test and glucose tolerance test. Altogether, these results suggest that BDNF Val66Met SNP strongly contributes to adipose tissue pathophysiology, resulting in reduced circulating leptin levels and hypothalamic expression of BDNF, which, in turn, promote increased food intake and overweight in BDNFMet/Met mice.本数据集包含与论文《BDNF Val66Met多态性改变小鼠摄食量与下丘脑BDNF表达》相关的原始数据。 **摘要** 肥胖作为日益严峻的公共卫生负担，属于多因素疾病，患者罹患2型糖尿病、高血压及心血管疾病等多种病理状态的风险显著升高。越来越多的证据表明，人脑源性神经营养因子（brain-derived neurotrophic factor，BDNF）Val66Met单核苷酸多态性（single-nucleotide polymorphism，SNP）与肥胖存在关联，但其具体作用机制尚未完全阐明。本研究发现，与野生型BDNFVal/Val小鼠相比，纯合敲入BDNFMet/Met小鼠存在体重超标与摄食过多的表型。在BDNFMet/Met小鼠的下丘脑中，摄食量增加与总BDNF以及BDNF1、BDNF4、BDNF6转录本的表达下调相关。与之相反，在BDNFMet/Met小鼠的白色脂肪组织中，总BDNF与葡萄糖转运蛋白4（Glut4）的表达水平上调，而沉默信息调节因子1（sirtuin 1）与瘦素受体（Ob-R）的表达水平则出现下调。此外，BDNFMet/Met小鼠的血浆瘦素水平有所降低。不过，BDNFVal/Val与BDNFMet/Met小鼠在胰岛素耐量试验与葡萄糖耐量试验中表现出相似的响应模式。综合来看，上述结果表明BDNF Val66Met单核苷酸多态性会显著影响脂肪组织的病理生理过程，导致循环瘦素水平下调以及下丘脑BDNF表达降低，进而促使BDNFMet/Met小鼠出现摄食量增加与体重超标的表型。