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

ABSTRACT: 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.

SUBMITTER: Mastaitis J 

PROVIDER: S-EPMC4330737 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature

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

Mastaitis Jason J   Min Soo S   Elvert Ralf R   Kannt Aimo A   Xin Yurong Y   Ochoa Francisca F   Gale Nicholas W NW   Valenzuela David M DM   Murphy Andrew J AJ   Yancopoulos George D GD   Gromada Jesper J  

Proceedings of the National Academy of Sciences of the United States of America 20150126 6

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  ...[more]

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