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) receptor agonists have emerged as highly effective therapies for obesity and type 2 diabetes by improving glycemic control and reducing body weight, primarily through the suppression of energy intake. Recent evidence suggests a bidirectional relationship between dietary intake and GLP-1 biology. Dietary factors, including caloric intake, meal timing, and macronutrient composition, may influence endogenous GLP-1 secretion, while GLP-1-based therapies may alter food choice and macronutrient preference. This review discusses the effects of dietary intake on endogenous GLP-1 regulation and examines how GLP-1-based therapies influence ingestive behavior and food preference, with particular emphasis on the responses to macronutrient composition. We further discuss the potential interaction between dietary intake and pharmacological GLP-1 signaling and its implications for metabolic health and aging. A better understanding of these bidirectional interactions may contribute to the development of personalized nutritional approaches that complement GLP-1-based therapies and improve long-term management of metabolic dysfunction. - Source: PubMed
Publication date: 2026/09/07
Han YerimShon JinyoungPark Yoon Jung - Periprosthetic osteolysis and aseptic loosening are the leading causes of total joint arthroplasty failure. Wear debris triggers chronic sterile inflammation, driving excessive osteoclast activation and insufficient osteoblastic bone formation. Drug-target Mendelian randomization showed that genetically predicted higher systemic expression of glucagon-like peptide-1 receptor (GLP-1R) is causally associated with a reduced risk of clinical revision arthroplasty. Histological analysis confirmed GLP-1R expression within osteolytic bone tissues. Whether local activation of GLP-1R could counter particle-induced osteolysis, however, remained untested. To address this, we evaluated the therapeutic potential of the GLP-1R agonist, Exendin-4, across animal models and in vitro assays. In a murine model of ultra-high-molecular-weight polyethylene (UHMWPE)-induced calvarial osteolysis, local Exendin-4 administration significantly mitigated bone resorption, suppressed osteoclastogenesis, and stimulated periprosthetic bone formation. Mechanistically, Exendin-4 shifted macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype, reducing osteolytic cytokines such as IL-6 and TNF-α; In vitro, it also acted directly on osteoclast precursors to suppress RANKL-driven osteoclastogenesis and rescued the osteogenic differentiation of bone marrow mesenchymal stem cells. These findings demonstrate that targeting GLP-1R signaling effectively restores the uncoupled bone homeostatic axis, offering a promising translational strategy for treating periprosthetic osteolysis. STATEMENT OF SIGNIFICANCE: Periprosthetic osteolysis (PPO) caused by wear debris is a major cause of joint replacement failure. While traditional treatments focus only on slowing down bone loss, strategies that can both stop bone destruction and promote bone healing are critically needed. In this study, we combined human genetic evidence with animal models to show that targeting the local GLP-1 receptor via Exendin-4 effectively treats PPO. Locally delivering Exendin-4 successfully switches pro-inflammatory M1 macrophages to an anti-inflammatory M2 phenotype and directly rescues the multi-stage bone formation process of stem cells under wear-particle stress, without causing systemic toxicity. This study provides a practical, biosafe strategy for reusing clinical metabolic drugs to balance bone remodeling and extend implant survival. - Source: PubMed
Publication date: 2026/09/05
Ma BoyanPeng ZhiPan YixiaoYi ZixiangSu Weiping - Colocalization analyses assess whether two traits are affected by the same or distinct causal genetic variants in a single gene region. A class of Bayesian enumeration colocalization tests are now routinely used in practice; for example, for genetic analyses in drug development pipelines. In this work, we consider an alternative frequentist approach to colocalization testing that examines the proportionality of genetic associations with each trait. The proportional colocalization approach uses markedly different assumptions to enumeration colocalization tests, and therefore can provide valuable complementary evidence in cases where enumeration colocalization results are inconclusive or sensitive to priors. We propose a novel conditional test of proportional colocalization, prop-coloc-cond, that aims to account for the uncertainty in variant selection, in order to recover accurate type I error control. The test can be implemented straightforwardly, requiring only summary data on genetic associations. Simulation evidence and an empirical investigation into GLP1R gene expression demonstrates how tests of proportional colocalization can offer important insights in conjunction with enumeration colocalization tests. - Source: PubMed
Publication date: 2026/09/04
Patel AshishWhittaker John CBurgess Stephen - - Source: PubMed
Publication date: 2026/09/03
Ramessur RaviSpindler ArchieMaas DerekCasagrande MaryGould Poppy AKhan AtlasShapiro JerryLo Sicco Kristen IPetukhova Lynn - Metabolic dysfunction-associated steatohepatitis (MASH), the progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD), is a heterogeneous and systemic disease that confers risk not only for cirrhosis and hepatocellular carcinoma (HCC) but also for extrahepatic complications including cardiovascular disease and chronic kidney disease. Over the past decade, numerous late-stage clinical trials have advanced the therapeutic landscape of MASH, culminating in a pivotal inflection point with accelerated approval of the thyroid hormone receptor-β (THRβ) agonist resmetirom and the glucagon-like peptide-1 receptor (GLP-1R) agonist semaglutide, establishing pharmacological options for patients with non-cirrhotic MASH and fibrosis. Concurrently, growing evidence indicates that MASH comprises distinct, partially overlapping disease subsets, ranging from liver-centric phenotypes with accelerated fibrogenesis and liver-related outcomes to cardiometabolic phenotypes characterized by insulin resistance and increased cardiovascular risk. This suggests that optimal treatment efficacy will require stratified and potentially combinatorial approaches. In addition to lifestyle interventions, a cornerstone of MASLD management, pharmacotherapies targeting metabolic dysfunction (including PPAR agonists, FGF21 analogues or incretin-based and glucagon-based therapies), fibrogenesis, inflammation and/or the gut-liver axis are emerging. In this Review, we summarize the therapeutic landscape for MASH and discuss how recent advances in disease phenotyping and biomarkers may enable a transition towards personalized therapy. - Source: PubMed
Publication date: 2026/09/02
Gallage SuchiraGovaere OlivierAnstee Quentin MShulman Gerald ITacke FrankHeikenwalder Mathias