Open AccessGPR17 gene disruption does not alter food intake or glucose homeostasis in mice
Author(s) -
Jason Mastaitis,
Soo Min,
Ralf Elvert,
Aimo Kannt,
Yurong Xin,
Francisca Ochoa,
Nicholas W. Gale,
David M. Valenzuela,
Andrew Murphy,
George D. Yancopoulos,
Jesper Gromada
Publication year - 2015
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1424968112
Subject(s) - glucose homeostasis , homeostasis , food intake , gene , biology , endocrinology , microbiology and biotechnology , medicine , genetics , diabetes mellitus , insulin resistance
G protein-coupled receptor 17 (GPR17) was recently reported to be a Foxo1 target in agouti-related peptide (AGRP) neurons. Intracerebroventricular 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.
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