ArticleThe Journal of clinical investigation2016
Disruption of Gpr45 causes reduced hypothalamic POMC expression and obesity.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Metabolic-inflammatory memory: the common pathological basis and therapeutic targets of metabolic syndrome.Reviews in endocrine & metabolic disorders · 2026Review
- International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.Pharmacological reviews · 2026Review
- Recent developments in GPCR signalling in appetite regulation.Bioscience reports · 2026Review
- Chemical cues and molecular mechanisms suspected in abiotic stress communication.The Journal of experimental biology · 2026Article
- Uncovering the role of Gpr45 in obesity regulation.Molecular metabolism · 2025Article
- GPR45 modulates GαScience (New York, N.Y.) · 2025Article
- Myristoylated Eepd1 Enhances Lipolysis and Thermogenesis through PKA Activation to Combat Obesity.Nature communications · 2025Article
- Exploring G Protein-Coupled Receptors in Hematological Cancers.ACS pharmacology & translational science · 2024Article
- Rare coding variant analysis for human diseases across biobanks and ancestries.Nature genetics · 2024Article
- Embryonic Lethal Phenotyping to Identify Candidate Genes Related with Birth Defects.International journal of molecular sciences · 2024Article
- Article
- Orphan G protein-coupled receptors: the ongoing search for a home.Frontiers in pharmacology · 2024Review
- Neurolysin Knockout Mice in a Diet-Induced Obesity Model.International journal of molecular sciences · 2023Article
- Advances in transposable elements: from mechanisms to applications in mammalian genomics.Frontiers in genetics · 2023Review
- A protein-coding gene expression atlas from the brain of pregnant and non-pregnant goats.Frontiers in genetics · 2023Article
- Article
- High-Throughput Screening of Mouse Gene Knockouts Identifies Established and Novel High Body Fat Phenotypes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- MicroRNA-188 regulates aging-associated metabolic phenotype.Aging cell · 2020Article
- Targeting hypoxia downstream signaling protein, CAIX, for CAR T-cell therapy against glioblastoma.Neuro-oncology · 2019Article
- Efficient genome-wide first-generation phenotypic screening system in mice using theProceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
A rise in the occurrence of obesity has driven exploration of its underlying genetic basis and potential targets for intervention. GWAS studies have identified obesity susceptibility pathways involving several neuropeptides that control energy homeostasis, suggesting that variations in the genes that regulate food intake and energy expenditure may contribute to obesity. In this study, we identified 5 additional obesity loci, including a neuronal orphan GPCR called Gpr45, in a forward genetic screen of mutant mice generated by piggyBac insertional mutagenesis. Disruption of Gpr45 led to increased adiposity at the time of weaning and increases in body mass, fat content, glucose intolerance, and hepatic steatosis with advancing age. Mice with disruptions in Gpr45 also displayed a reduction in expression of the metabolic regulator POMC and less energy expenditure prior to the onset of obesity. Mechanistically, we determined that GPR45 regulates POMC expression via the JAK/STAT pathway in a cell-autonomous manner. Consistent with this finding, intraventricular administration of melanotan-2, an analog of the POMC derivative α-MSH, suppressed adult obesity in Gpr45 mutants. These results reveal that GPR45 is a regulator of POMC signaling and energy expenditure, which suggests that it may be a potential intervention target to combat obesity.
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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.