Gpr149 is involved in energy homeostasis in the male mouse.
Gpr149 is involved in energy homeostasis in the male mouse.
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作者：
Wyler S;Surbhi;Cao N;Merchant W;Bookout A;Gautron L
GPR149是一种孤儿受体，人们对其知之甚少。因此，在本研究中，我们使用了三种互补的方法来定位Gpr149在小鼠中的组织表达：定量PCR、原位杂交和新产生的Gpr149-Cre报告小鼠模型。Gpr149在Calleja岛、下丘脑腹内侧核和吻侧脚间核的神经元中表达最强。在基底前脑、纹状体、下丘脑、脑干和脊髓也观察到中低水平的表达。Gpr149在初级传入神经元、肠神经元和垂体内分泌细胞中也有表达。这种表达模式与GPR149信号参与能量平衡的调节是一致的。为了探讨GPR149在体内的生理功能，我们使用CRISPR-CAS9对缺乏GPR149外显子1的小鼠产生了一个全局敲除等位基因。初步的代谢研究表明，GPR149−/−小鼠在高脂饮食中部分抵抗体重增加，并且比对照小鼠对胰岛素更敏感。综上所述，我们的数据可以作为未来饮食诱导肥胖背景下GPR149的活体研究的资源。
GPR149 is an orphan receptor about which little is known. Accordingly, in the present study, we mapped the tissue expression of Gpr149 in mice using three complementary approaches: quantitative PCR, in situ hybridization, and a newly generated Gpr149-Cre reporter mouse model. The strongest expressions of Gpr149 were observed in neurons of the islands of Calleja, the ventromedial hypothalamus, and the rostral interpeduncular nucleus. Moderate-to-low expression was also observed in the basal forebrain, striatum, hypothalamus, brainstem, and spinal cord. Some Gpr149 expression was also detected in the primary afferent neurons, enteric neurons, and pituitary endocrine cells. This expression pattern is consistent with the involvement of GPR149 signaling in the regulation of energy balance. To explore the physiological function of GPR149 in vivo, we used CRISPR-Cas9 to generate a global knockout allele with mice lacking Gpr149 exon 1. Preliminary metabolic findings indicated that Gpr149−/− mice partially resist weight gain when fed with a high-fat diet and have greater sensitivity to insulin than control mice. In summary, our data may serve as a resource for future in vivo studies on GPR149 in the context of diet-induced obesity.
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影响因子：
16.2
作者：
Dhillon, H;Zigman, JM;Lowelll, BB
通讯作者：
Lowelll, BB
影响因子：
8.1
作者：
Burke LK;Ogunnowo-Bada E;Georgescu T;Cristiano C;de Morentin PBM;Valencia Torres L;D'Agostino G;Riches C;Heeley N;Ruan Y;Rubinstein M;Low MJ;Myers MG;Rochford JJ;Evans ML;Heisler LK
通讯作者：
Heisler LK
影响因子：
25
作者：
Madisen L;Zwingman TA;Sunkin SM;Oh SW;Zariwala HA;Gu H;Ng LL;Palmiter RD;Hawrylycz MJ;Jones AR;Lein ES;Zeng H
通讯作者：
Zeng H
影响因子：
8.2
作者：
Sánchez-Garrido MA;Brandt SJ;Clemmensen C;Müller TD;DiMarchi RD;Tschöp MH
通讯作者：
Tschöp MH
影响因子：
7.7
作者：
Affinati AH;Sabatini PV;True C;Tomlinson AJ;Kirigiti M;Lindsley SR;Li C;Olson DP;Kievit P;Myers MG;Rupp AC
通讯作者：
Rupp AC