The present study was carried out to see possible involvement of G-protein-coupled estrogen receptor 1 (GPER, GPR30) to glucose metabolism.  To this end, rats were ovariectomized and were primed with the silicone tube containing cholesterol, 17b-Estradiol, or GPER selective agonist G1.  Firstly, we revealed tahat G1 agonist did not have estrogenic action in reproductive system like estrogen did: G1 treatment did not show uterotropic action, positive and negative feedback effects on gonadotropin secretions.  These results suggest that GPER does not have any effects on the reproductive system.  G1 treatment did not show any effects on open field, body weight, food amounts to eat like estrogen did, and these results lead us to conclude that GPER did not play a role on behaviors controlled by the central nervous system.  However, we found that G1 treatment selectively worse the glucose tolerance test.  Since G1 agonist did not affect O₂ consumption, and NPY neurons have specific role on the glucose tolerance test, we speculate this G1 effect was via NPY neurons.  In fact, we found that some NPY neurons in the arcuate nucleus of the hypothalamus also expressed GPER immunoreactivity.  We also found in a expression array experiment that platelet-derived growth factor receptor-alpha (PDGFR-a) mRNA was specifically upregulated by G1 treatment but not estrogen.  Also, G1 treatment increased the protein of PDGFR-a in the hypothalamus.  Thus we hypothesized that GPER expressed in NPY neurons affected glucose tolerance via a acting at PDGFR-a.