ArticleThe Journal of clinical investigation2016
Hypomorphism of Fto and Rpgrip1l causes obesity in mice.
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 57 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- Pooled it
- Mendelian pathway analysis of laboratory traits reveals distinct roles for ciliary subcompartments in common disease pathogenesis.American journal of human genetics · 2021Pooled it
- Effect direction meta-analysis of GWAS identifies extreme, prevalent and shared pleiotropy in a large mammal.Communications biology · 2020Pooled it
- The genetics of obesity: aetiology, prevention and therapy.Nature metabolism · 2026Review
- NBiomolecules · 2026Review
- Primary cilia in osteoblasts and osteocytes are required for skeletal development and mechano-adaptation.PloS one · 2026Article
- FTO-Mediated m6A Demethylation in Insulin Resistance and Type 2 Diabetes: Tissue-Specific Mechanisms - a Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Circulating FTO Protein Levels and β-Cell Function in Individuals with Different Metabolic Profiles: A Cross- Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- The Clinical Relevance of FTO as a Demethylase Beyond Cancer: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- FTO promotes weight gain via altering Kif1a splicing and axonal vesicle trafficking in AgRP neurons.The EMBO journal · 2025Article
- Association between FTO gene polymorphism and obesity in down syndrome children.European journal of pediatrics · 2024Article
- Risk of Fat Mass- and Obesity-Associated Gene-Dependent Obesogenic Programming by Formula Feeding Compared to Breastfeeding.Nutrients · 2024Review
- Endocrine, genetic, and microbiome nexus of obesity and potential role of postbiotics: a narrative review.Eating and weight disorders : EWD · 2023Review
- Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
- Neuronal primary cilia integrate peripheral signals with metabolic drives.Frontiers in physiology · 2023Review
- Unraveling the Complex Interactions between the Fat Mass and Obesity-Associated (FTO) Gene, Lifestyle, and Cancer.Advances in nutrition (Bethesda, Md.) · 2022Review
- Clock genes rescue nphp mutations in zebrafish.Human molecular genetics · 2022Article
- Mechanisms of Weight Control by Primary Cilia.Molecules and cells · 2022Review
- The genetics of obesity: from discovery to biology.Nature reviews. Genetics · 2022Review
- The effect of FTO rs9939609 polymorphism on the association between colorectal cancer and dietary fiber.Frontiers in nutrition · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Noncoding polymorphisms in the fat mass and obesity-associated (FTO) gene represent common alleles that are strongly associated with effects on food intake and adiposity in humans. Previous studies have suggested that the obesity-risk allele rs8050136 in the first intron of FTO alters a regulatory element recognized by the transcription factor CUX1, thereby leading to decreased expression of FTO and retinitis pigmentosa GTPase regulator-interacting protein-1 like (RPGRIP1L). Here, we evaluated the effects of rs8050136 and another potential CUX1 element in rs1421085 on expression of nearby genes in human induced pluripotent stem cell-derived (iPSC-derived) neurons. There were allele-dosage effects on FTO, RPGRIP1L, and AKT-interacting protein (AKTIP) expression, but expression of other vicinal genes, including IRX3, IRX5, and RBL2, which have been implicated in mediating functional effects, was not altered. In vivo manipulation of CUX1, Fto, and/or Rpgrip1l expression in mice affected adiposity in a manner that was consistent with CUX1 influence on adiposity via remote effects on Fto and Rpgrip1l expression. In support of a mechanism, mice hypomorphic for Rpgrip1l exhibited hyperphagic obesity, as the result of diminished leptin sensitivity in Leprb-expressing neurons. Together, the results of this study indicate that the effects of FTO-associated SNPs on energy homeostasis are due in part to the effects of these genetic variations on hypothalamic FTO, RPGRIP1L, and possibly other genes.
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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.