ArticleObesity (Silver Spring, Md.)2023
Gpr75-deficient mice are protected from high-fat diet-induced obesity.
Article in Obesity (Silver Spring, Md.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Global GPR75 deficiency protects against diet-induced obesity through central and peripheral mechanisms.Molecular metabolism · 2026Article
- G protein-coupled receptor 75 mediates depression-like behaviors and HPA axis hyperactivity through an excitatory arcuate-paraventricular nucleus circuit.Acta pharmacologica Sinica · 2026Article
- The evolving landscape of obesity pharmacotherapy.Nature reviews. Drug discovery · 2026Review
- Recent developments in GPCR signalling in appetite regulation.Bioscience reports · 2026Review
- GPR75 genetic manipulations in mice reveal central mechanism for weight loss independent of developmental effects.Molecular metabolism · 2026Article
- Cryo-EM structures of GPR75 reveal an occluded orthosteric pocket challenging conventional drug discovery paradigms for an anti-obesity target.Acta pharmacologica Sinica · 2026Article
- Inhibition of GPR75 Alleviates Lipid Metabolism by Activating the AMPK-SIRT1 Signaling Pathway In Vitro and In Vivo.Molecular biotechnology · 2026Article
- GPR75 in glutamatergic neurons regulates body weight.Cell reports · 2026Article
- Gpr75 Deletion in Adipocytes Protects From Diet-Induced Obesity: Changes in Glucose Homeostasis and Inflammatory Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Anatomical and Neuronal Distribution of the G-Coupled Protein Receptor 75 mRNA in the Mouse Central Nervous System.The European journal of neuroscience · 2026Article
- Neuronal GPR75 deficiency protects against diet-induced obesity in a humanized mouse model.Science advances · 2026Article
- Cell membrane-coated nanoparticles against non-alcoholic fatty liver disease via regulating endoplasmic reticulum stress.Regenerative biomaterials · 2026Article
- GPR75 signaling is dispensable for reproduction but contributes to feeding and body growth in rats on normal chow and is involved in high-fat diet-induced hyperphagia, obesity, and hyperglycemia development.Endocrine journal · 2025Article
- Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025Review
- Effects of pyruvate administration on mRNA expression of inflammatory cytokines in adipose tissue and whole-body glucose metabolism in male mice.Physiological reports · 2025Article
- GPR75: Advances, Challenges in Deorphanization, and Potential as a Novel Drug Target for Disease Treatment.International journal of molecular sciences · 2025Review
- The expanding landscape of genetic causes of obesity.Pediatric research · 2025Review
- Adopting GPR75 in treating obesity: unraveling the knowns and unknowns of this orphan GPCR.Trends in cell biology · 2025Review
- Ciliary localization of GPR75 promotes fat accumulation in mice.The Journal of clinical investigation · 2024Article
- Central regulation of feeding and body weight by ciliary GPR75.The Journal of clinical investigation · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveG-protein coupled receptor 75 (GPR75) has been identified as the high-affinity receptor of 20-hydroxyeicosatetraenoic acid (20-HETE), a vasoactive and proinflammatory lipid, and mice overproducing 20-HETE have been shown to develop insulin resistance when fed a high-fat diet (HFD), which was prevented by a 20-HETE receptor blocker. Simultaneously, a large-scale exome sequencing of 640,000 subjects identified an association between loss-of-function GPR75 variants and protection against obesity.
methodsWild-type (WT) and Gpr75-deficient mice were placed on HFD for 14 weeks, and their obesity phenotype was examined.
resultsMale and female Gpr75 null (knockout [KO]) and heterozygous mice gained less weight than WT mice when placed on HFD. KO mice maintained the same level of energy expenditure during HFD feeding, whereas WT mice showed a significant reduction in energy expenditure. Diet-driven adiposity and adipocyte hypertrophy were greatly lessened in Gpr75-deficient mice. HFD-fed KO mice did not develop insulin resistance. Adipose tissue from Gpr75-deficient mice had increased expression of thermogenic genes and decreased levels of inflammatory markers. Moreover, insulin signaling, which was impaired in HFD-fed WT mice, was unchanged in KO mice.
conclusionsThese findings suggest that GPR75 is an important player in the control of metabolism and glucose homeostasis and a likely novel therapeutic target to combat obesity-driven metabolic disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.