GPR17 gene disruption does not alter food intake or glucose homeostasis in mice

被引:19
作者
Mastaitis, Jason [1 ]
Min, Soo [1 ]
Elvert, Ralf [2 ]
Kannt, Aimo [2 ]
Xin, Yurong [1 ]
Ochoa, Francisca [1 ]
Gale, Nicholas W. [1 ]
Valenzuela, David M. [1 ]
Murphy, Andrew J. [1 ]
Yancopoulos, George D. [1 ]
Gromada, Jesper [1 ]
机构
[1] Regeneron Pharmaceut Inc, Tarrytown, NY 10591 USA
[2] Sanofi Diabet Res & Translat Med, D-65926 Frankfurt, Germany
关键词
GPR17; AGRP; diabetes; body weight; food intake; AGOUTI-RELATED PROTEIN; EXPRESSION ANALYSIS; INVERSE AGONIST; RECEPTOR GPR17; NEURONS; AGRP; LEPTIN; FOXO1; LEUKOTRIENES; INSULIN;
D O I
10.1073/pnas.1424968112
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
G protein-coupled receptor 17 (GPR17) was recently reported to be a Foxo1 target in agouti-related peptide (AGRP) neurons. Intra-cerebroventricular injection of GPR17 agonists induced food intake, whereas administration of an antagonist to the receptor reduced feeding. These data lead to the conclusion that pharmacological modulation of GPR17 has therapeutic potential to treat obesity. Here we report that mice deficient in Gpr17 (Gpr17(-/-)) have similar food intake and body weight compared with their wild-type littermates. Gpr17(-/-) mice have normal hypothalamic Agrp mRNA expression, AGRP plasma levels, and metabolic rate. GPR17 deficiency in mice did not affect glucose homeostasis or prevent fat-induced insulin resistance. These data do not support a role for GPR17 in the control of food intake, body weight, or glycemic control.
引用
收藏
页码:1845 / 1849
页数:5
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