GLP1R Antibody
- Known as:
- GLP1R Antibody
- Catalog number:
- csb-pa009514la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- GLP1R Antibody
Related genes to: GLP1R Antibody
- Gene:
- GLP1R NIH gene
- Name:
- glucagon like peptide 1 receptor
- Previous symbol:
- -
- Synonyms:
- GLP-1R
- Chromosome:
- 6p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-11
- Date modifiied:
- 2017-02-07
Related products to: GLP1R Antibody
Related articles to: GLP1R Antibody
- Glucagon-like peptide-1 (GLP-1) in the brain is synthesized by preproglucagon neurons and released through axonal projections to extensive regions such as the arcuate nucleus, hypothalamic paraventricular nucleus (PVN), rostral ventrolateral medulla, and dorsomedial medulla. It is involved in functional activities including substance metabolism, neuroendocrine regulation, and autonomic nerve control. The GLP-1 receptor (GLP-1R) is highly expressed in the PVN and plays an important role in stress responses and cardiovascular activities. However, the mechanism by which GLP-1 influences the activity of magnocellular neurosecretory cells (MNCs) in the hypothalamic PVN remains unclear. In this study, we used whole-cell patch-clamp recording in acute hypothalamic slices, biotin staining, double immunofluorescence staining, and neuropharmacology methods to investigate the regulatory mechanism of GLP-1 on the activity of the hypothalamic PVN MNCs in rats. Under current-clamp conditions, perfusion with GLP-1 (100 nmol/L) resulted in a significant decrease in the spontaneous firing frequency of PVN MNCs accompanied with a membrane potential hyperpolarization. Blocking ionotropic glutamate receptors and GABA receptors either alone or simultaneously did not affect the inhibitory effect of GLP-1 on the firing frequency of PVN MNCs. GLP-1 had no significant impact on the half-width, rise constant, or decay constant of action potentials, but it significantly increased the after-hyperpolarization (AHP) and inwardly rectifying potassium currents of PVN MNCs. The results of double immunofluorescence showed that GLP-1 significantly reduced the expression of c-fos in arginine vasopressin (AVP)-ergic neurons. These results indicate that GLP-1 activates postsynaptic inwardly rectifying potassium channels, reduces the excitability of PVN MNCs, and decreases their firing frequency and c-fos expression. These findings suggest that GLP-1 reduces the secretion and release of AVP by inhibiting the functional activity of PVN MNCs in rats. - Source: PubMed
Jin XinChen LiChu Chun-PingLi Yu-ZiRen PengQiu De-Lai - The migrating myoelectric complex (MMC) is the electrical basis of fasting small intestinal motility. Although oxytocin (OT) regulates gastrointestinal functions through oxytocin receptors (OTRs), its effect on jejunal MMC activity during fasting remains unclear. This study investigated the effects of OT on jejunal MMC activity in fasted rats and evaluated the involvement of OTRs, glucagon-like peptide-1 receptors (GLP-1Rs), and nitric oxide (NO) pathways. Bipolar electrodes were implanted at three jejunal sites in adult male Sprague Dawley rats for MMC recordings. After recovery and 18 h fasting, OT was administered intraperitoneally (4-32 µg/kg) following one hour of basal recording. To assess mechanisms, rats were pretreated with the OTR antagonist atosiban (2 mg/kg), the GLP-1R antagonist exendin (9-39) (200 µg/kg), or the nitric oxide synthase inhibitor NG-nitro-L-arginine (L-NNA; 5 mg/kg) before OT (16 µg/kg). Oxytocin dose-dependently reduced spike frequency and MMC cycle number ( < 0.05-0.001 vs. vehicle). Atosiban completely reversed these effects ( < 0.001 vs. OT), while exendin (9-39) partially attenuated them ( < 0.01-0.001 vs. OT). L-NNA showed no significant effect. These findings indicate that OT inhibits jejunal MMC activity via OTR-dependent mechanisms with partial involvement of GLP-1R signaling but not NO pathways. - Source: PubMed
Publication date: 2026/06/19
Balcı HakanSaltık Özge DarakcıAktemur Burcu HatipoğluAbdullahoğlu RümeysaBozkurt Ayhan - The dual agonism of glucagon-like peptide-1 receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide receptor (GIPR) becomes a groundbreaking treatment for type 2 diabetes (T2D) that achieves robust glycemic control and maintains body weight. It also induces potential risk reduction in diabetic retinopathy (DR), Alzheimer disease (AD), and heart diseases including coronary artery disease (CAD) in treated T2D patients. To date, the molecular basis underpinning the remarkable causal treatment effects and synergy of the dual agonism of GLP-1R and GIPR on risk reduction in T2D, CAD, DR and AD has not been systematically investigated. To elucidate the treatment effects and potential synergy of dual GLP-1R/GIPR agonism on risk reduction in T2D, CAD, DR and AD while minimizing the impact of confounders, we used a robust cis-Mendelian randomization (cis-MR) with a principal component-based generalized method of moments (PC-GMM) where blood-based glycated hemoglobin (HbA1c), high- and low-density lipoprotein cholesterol (HDL-c, LDL-c), and BMI were used as mediating biomarkers. Our cis-MR analyses confirmed a synergistic causal protective effect of dual GLP-1R/GIPR agonism on T2D via HbA1c reduction [OR = 0.17; 95% CI = (0.11, 0.26); = 3.68 × 10] which is more significant than either GLP-1R agonism or GIPR agonism alone. Similarly, the causal protective effect of dual GLP-1R/GIPR agonism via HbA1c reduction was also significant for DR [OR = 0.20; 95% CI = (0.11, 0.36); = 9.22 × 10]. Further, our multivariate cis-MR (or cis-MVMR) analyses revealed that after adjusting for HbA1c, a synergistic protective effect on DR via a reduction in LDL-c is significant in dual GLP-1R/GIPR agonism [OR = 0.57; 95% CI = (0.29, 0.94)], while the protective effect on DR of LDL-c reduction is non-significant in either GLP-1R agonism or GIPR agonism alone. Also, after adjusting for HbA1c, the multivariate cis-MR results showed significant protective effects on AD via a reduction in LDL-c in GLP-1R/GIPR agonism [OR = 0.44; 95% CI = (0.25, 0.81)]. Importantly, the multivariate cis-MR results also revealed that dual GLP-1R/GIPR agonism has significant protective effects on CAD via both a reduction in BMI [OR = 0.46; 95% CI = (0.28, 0.75)] and an improvement in HDL [OR = 0.59; 95% CI = (0.39, 0.90)]. This is in support of the hypothesis that dual GLP-1R/GIPR agonism has a synergistic protective effect on CAD that is stronger than that of GLP-1R agonism alone, which yielded a non-significant causal effect for both HDL and BMI, and GIPR agonism alone also yielded a non-significant causal effect for HDL when adjusted for BMI. These novel findings have significant implications for repurposing dual incretin agonism in terms of diabetic drugs to serve as a unifying, precision prevention strategy against CAD, DR and AD as leading drivers of mortality and morbidity in diabetic patients. - Source: PubMed
Publication date: 2026/05/25
Xu JiehuiAshebir Yibeltal AShao Yongzhao - Fermentation is widely used to enhance the bioactivity of herbal phytochemicals through microbial bioconversion. contains catalpol, an iridoid glycoside with metabolic and immunomodulatory potential; however, its efficacy in the unfermented form is limited. This study investigated whether fermentation enhances catalpol production and improves metabolic and immune-regulating functions via glucagon-like peptide-1 receptor (GLP-1R) signaling. extract was fermented under optimized conditions, and catalpol and iridoid precursor levels were quantified to assess bioconversion efficiency. Biological effects were evaluated in intestinal epithelial cells, macrophages, and an Artemia model, focusing on glucose transport, GLP-1 secretion, dipeptidyl peptidase-4 (DPP-4) expression, mucosal defense, and GLP-1R/protein kinase A/cAMP response element-binding protein (PKA/CREB) signaling. Fermentation significantly increased catalpol content while reducing iridoid precursors. The fermented extract suppressed intestinal glucose absorption by downregulating sodium-glucose cotransporter 1 (SGLT1) and glucose transporter 2 (GLUT2). It also enhanced GLP-1 secretion and reduced DPP-4 expression, leading to activation of GLP-1R/PKA/CREB signaling. This activation increased mucin 2 (MUC2) expression and promoted anti-inflammatory. - Source: PubMed
Publication date: 2026/05/26
You Eun-JiKim Boyong - The glucagon-like peptide-1 receptor (GLP-1R) is a class B G protein-coupled receptor (GPCR) central to metabolic regulation, and its potential modulation by dietary phytochemicals is increasingly recognized as physiologically relevant. Understanding how such compounds interact with GLP-1R is important for clarifying mechanisms that may contribute to gut-to-brain signaling. In this study, we examined three structurally related dietary ginsenosides, Rg1, Rg2, and Rg3, as potential modulators of GLP-1R using luciferase reporter assays and computational analyses. Despite sharing similar molecular weights, a common dammarane scaffold, and comparable sugar moieties, the three ginsenosides displayed distinct effects on GLP-1R activity: Rg2 and Rg3 potently reduced receptor activation in a dose-dependent manner when co-administered with Exendin-4, whereas Rg1 had minimal effect. Computational screening of the GLP-1R structure for binding sites identified a putative extracellular pocket on the protein that can accommodate these compounds, while molecular docking and binding free energy calculations provided predicted affinities qualitatively reflecting the phytochemicals' experimental activities. These findings point to a plausible extracellular mechanism through which dietary ginsenosides may influence GLP-1R responsiveness at the intestinal interface. Our results point to the possibility that non-absorbed phytochemicals can differentially modulate gut-expressed receptors, suggesting a novel pathway for dietary signaling relevant to ethnopharmacology and metabolic health. - Source: PubMed
Publication date: 2026/06/22
Caspi AyeletKhazanov NetalyHelman AharonLankry HodayaLevavi-Sivan BertaSenderowitz HanochKerem Zohar