ArticleTranslational psychiatry2013
Moderation of antipsychotic-induced weight gain by energy balance gene variants in the RUPP autism network risperidone studies.
Article in Translational psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.
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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
23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Atypical antipsychotics for autism spectrum disorder: a network meta-analysis.The Cochrane database of systematic reviews · 2025Pooled it
- Pharmacogenomic Studies in Intellectual Disabilities and Autism Spectrum Disorder: A Systematic Review.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2021Pooled it
- Genome-wide association study on antipsychotic-induced weight gain in the CATIE sample.The pharmacogenomics journal · 2016Pooled it
- Weight Gain and Metabolic Consequences of Risperidone in Young Children With Autism Spectrum Disorder.Journal of the American Academy of Child and Adolescent Psychiatry · 2016Trial
- Pharmacogenomics of risperidone in autism spectrum disorder: a minireview.Frontiers in pharmacology · 2026Review
- Clinical Utility and Implementation of Pharmacogenomics for the Personalisation of Antipsychotic Treatments.Pharmaceutics · 2024Review
- Glucose and Lipid Profiles Predict Anthropometric Changes in Drug-Naïve Adolescents Starting Treatment with Risperidone or Sertraline: A Pilot Study.Biomedicines · 2022Article
- TheCurrent developments in nutrition · 2022Article
- Association of CNR1 and INSIG2 polymorphisms with antipsychotics-induced weight gain: a prospective nested case-control study.Scientific reports · 2021Article
- Search for Possible Associations ofPharmacogenomics and personalized medicine · 2021Article
- The Burden of Antipsychotic-Induced Weight Gain and Metabolic Syndrome in Children.Frontiers in psychiatry · 2021Review
- Pharmacogenomic Characterization in Bipolar Spectrum Disorders.Pharmaceutics · 2019Review
- Pharmacogenetic Correlates of Antipsychotic-Induced Weight Gain in the Chinese Population.Neuroscience bulletin · 2019Review
- Genetic validation study of protein tyrosine phosphatase receptor type D (PTPRD) gene variants and risk for antipsychotic-induced weight gain.Journal of neural transmission (Vienna, Austria : 1996) · 2019Article
- Associations between theMolecular neuropsychiatry · 2018Article
- Audit of physical health monitoring in children and adolescents receiving antipsychotics in neurodevelopmental clinics in Northumberland.World journal of psychiatry · 2018Article
- Autism genetics: opportunities and challenges for clinical translation.Nature reviews. Genetics · 2017Review
- Serum metabolite profile associates with the development of metabolic co-morbidities in first-episode psychosis.Translational psychiatry · 2016Article
- Genetics of Common Antipsychotic-Induced Adverse Effects.Molecular neuropsychiatry · 2016Review
- Association Study of Serotonin 3 Receptor Subunit Gene Variants in Antipsychotic-Induced Weight Gain.Neuropsychobiology · 2016Article
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 1 country.
Funding
Abstract
Second-generation antipsychotic exposure, in both children and adults, carries significant risk for excessive weight gain that varies widely across individuals. We queried common variation in key energy balance genes (FTO, MC4R, LEP, CNR1, FAAH) for their association with weight gain during the initial 8 weeks in the two NIMH Research Units on Pediatric Psychopharmacology Autism Network trials (N=225) of risperidone for treatment of irritability in children/adolescents aged 4-17 years with autism spectrum disorders. Variants in the cannabinoid receptor (CNR)-1 promoter (P=1.0 × 10(-6)), CNR1 (P=9.6 × 10(-5)) and the leptin (LEP) promoter (P=1.4 × 10(-4)) conferred robust-independent risks for weight gain. A model combining these three variants was highly significant (P=1.3 × 10(-9)) with a 0.85 effect size between lowest and highest risk groups. All results survived correction for multiple testing and were not dependent on dose, plasma level or ethnicity. We found no evidence for association with a reported functional variant in the endocannabinoid metabolic enzyme, fatty acid amide hydrolase, whereas body mass index-associated single-nucleotide polymorphisms in FTO and MC4R showed only trend associations. These data suggest a substantial genetic contribution of common variants in energy balance regulatory genes to individual antipsychotic-associated weight gain in children and adolescents, which supersedes findings from prior adult studies. The effects are robust enough to be detected after only 8 weeks and are more prominent in this largely treatment naive population. This study highlights compelling directions for further exploration of the pharmacogenetic basis of this concerning multifactorial adverse event.
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