ArticleInternational journal of obesity (2005)2016
16p11.2 Locus modulates response to satiety before the onset of obesity.
Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Multidimensional Characterisation of Eating Behaviour in Genetic Obesity: A Systematic Review.Obesity facts · 2026Pooled it
- Long-term effects of bariatric surgery in patients with obesity and chromosome 16 p11.2 microdeletion.Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery · 2017Trial
- Article
- Integrating genetic and transcriptomic data to identify genes underlying obesity risk loci.International journal of obesity (2005) · 2025Article
- TAOK2 drives opposing cilia length deficits in 16p11.2 deletion and duplication carriers.Stem cell reports · 2025Article
- Developmental milestones and cognitive trajectories in school-aged children with 16p11.2 deletion.Journal of neurodevelopmental disorders · 2025Article
- Eating behaviour and eating disorders in individuals with rare neurodevelopmental variants: current knowledge and future research directions.Frontiers in psychiatry · 2025Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Language Profiles of School-Age Children With 16p11.2 Copy Number Variants in a Clinically Ascertained Cohort.Journal of speech, language, and hearing research : JSLHR · 2024Article
- Experiences and concerns of parents of children with a 16p11.2 deletion or duplication diagnosis: a reflexive thematic analysis.BMC psychology · 2024Article
- Hyperphagia and impulsivity: use of self-administered Dykens' and in-house impulsivity questionnaires to characterize eating behaviors in children with severe and early-onset obesity.Orphanet journal of rare diseases · 2024Article
- Association between increased BMI and cognitive function in first-episode drug-naïve male schizophrenia.Frontiers in psychiatry · 2024Article
- Genomic deletions on 16p11.2 associated with severe obesity in Brazil.Frontiers in endocrinology · 2024Article
- Health supervision for children and adolescents with 16p11.2 deletion syndrome.Cold Spring Harbor molecular case studies · 2023Article
- Current Treatments for Patients with Genetic ObesityJournal of clinical research in pediatric endocrinology · 2023Review
- Article
- Clinical evaluation of patients with a neuropsychiatric risk copy number variant.Current opinion in genetics & development · 2021Review
- Touch and olfaction/taste differentiate children carrying a 16p11.2 deletion from children with ASD.Molecular autism · 2021Article
- Appetitive traits as targets for weight loss: The role of food cue responsiveness and satiety responsiveness.Physiology & behavior · 2020Review
- The Role of Genetic Variation of BMI, Body Composition, and Fat Distribution for Mental Traits and Disorders: A Look-Up and Mendelian Randomization Study.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
29 authors at 11 institutions in 6 countries.
Funding
Abstract
backgroundThe 600 kb BP4-BP5 copy number variants (CNVs) at the 16p11.2 locus have been associated with a range of neurodevelopmental conditions including autism spectrum disorders and schizophrenia. The number of genomic copies in this region is inversely correlated with body mass index (BMI): the deletion is associated with a highly penetrant form of obesity (present in 50% of carriers by the age of 7 years and in 70% of adults), and the duplication with being underweight. Mechanisms underlying this energy imbalance remain unknown.
objectiveThis study aims to investigate eating behavior, cognitive traits and their relationships with BMI in carriers of 16p11.2 CNVs.
methodsWe assessed individuals carrying a 16p11.2 deletion or duplication and their intrafamilial controls using food-related behavior questionnaires and cognitive measures. We also compared these carriers with cohorts of individuals presenting with obesity, binge eating disorder or bulimia.
resultsResponse to satiety is gene dosage-dependent in pediatric CNV carriers. Altered satiety response is present in young deletion carriers before the onset of obesity. It remains altered in adolescent carriers and correlates with obesity. Adult deletion carriers exhibit eating behavior similar to that seen in a cohort of obesity without eating disorders such as bulimia or binge eating. None of the cognitive measures are associated with eating behavior or BMI.
conclusionsThese findings suggest that abnormal satiety response is a strong contributor to the energy imbalance in 16p11.2 CNV carriers, and, akin to other genetic forms of obesity, altered satiety responsiveness in children precedes the increase in BMI observed later in adolescence.
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