Chemerin and GPR1 show increased on serum and placental in mice during pregnancy. Interestingly, we observed increased serum chemerin levels and decreased GPR1 expression in HFD-fed mice placental compared to chow at GD 18. GPR1 protein and gene levels were significantly decreased in GDM patient placentas. It was previously reported that serum chemerin levels are markedly increased in obese and gestational diabetes mellitus (GDM) patients and positively associated with the risk of GDM in the first trimester, and loss of GPR1, a chemerin receptor, could result in glucose intolerance in obese mice. Therefore, we hypothesized that chemerin/GPR1 signaling might participate in the pathogenic mechanism of GDM. Our study is the first report on the expression of GPR1, and on the characterization of its direct biological effects in humans and mice, including the molecular mechanism that indicates the role of GPR1 signaling in maternal metabolism during pregnancy. Decreased GPR1 levels were measured in GDM patient placentas. Meanwhile, it was confirmed that GPR1 knockdown exacerbated glucose intolerance and disrupted lipid metabolism. These findings indicate a novel feedback mechanism to regulate glucose balance during pregnancy, and GPR1 could be a potential target for the detection, prevention, and therapy of GDM.

MRI and PET are important modalities and can provide complementary information for the diagnosis of brain diseases because MRI can provide structural information of brain and PET can obtain functional information of brain. However, PET is usually missing. Especially, simultaneous PET and MRI imaging at ultrahigh field is not achievable in the current. Thus, synthetic PET using MRI at ultrahigh field is essential. In this paper, we synthetic PET using MRI as a guide by joint probability distribution of diffusion model (JPDDM). Meanwhile, We utilized our model in Ultrahigh Fields.