ArticleItalian journal of pediatrics2010
Chromosome 16p11.2 deletions: another piece in the genetic puzzle of childhood obesity.
Article in Italian journal of pediatrics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Neurodevelopmental copy-number variants increase risk of internalizing and cardiometabolic multimorbidity: Findings from the UK Biobank.American journal of human genetics · 2026Article
- Exploring Autosomal Dominant Non-Syndromic Monogenic Obesity: From Genes to Therapy.Current issues in molecular biology · 2026Review
- Genetic architecture of obesity and advances in precision pharmacotherapy: a comprehensive review.Acta biochimica Polonica · 2026Review
- Integrating genetic and transcriptomic data to identify genes underlying obesity risk loci.International journal of obesity (2005) · 2025Article
- Health supervision for children and adolescents with 16p11.2 deletion syndrome.Cold Spring Harbor molecular case studies · 2023Article
- Reviewed and updated Algorithm for Genetic Characterization of Syndromic Obesity Phenotypes.Current genomics · 2022Review
- Phosphorylation of the Unique C-Terminal Tail of the Alpha Isoform of the Scaffold Protein SH2B1 Controls the Ability of SH2B1α To Enhance Nerve Growth Factor Function.Molecular and cellular biology · 2018Article
- Understanding the pathophysiological mechanisms in the pediatric non-alcoholic fatty liver disease: The role of genetics.World journal of hepatology · 2015Article
- Article
- Recent advances in obesity: genetics and beyond.ISRN endocrinology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ipercaloric diet and reduced physical activity have driven the rise in the prevalence of childhood obesity over a relatively short time interval. Family and twin studies have led to the conclusion that the strong predictive value of parental body mass index (BMI) mainly stems from genetic rather than environmental factors. Whereas the common polygenic obesity arises when an individual genetic make-up is susceptible to an environment that promotes energy consumption over energy expenditure, monogenic obesity, on the contrary, is the obesity associated with a single gene mutation, which is sufficient by itself to cause weight gain in a food abundant context. Genes involved in the leptin-melanocortin pathway are often mutated in these cases. The cumulative prevalence of monogenic obesity among children with severe obesity is about 5%. Recently, deletions in the region p11.2 of the chromosome 16 encompassing the gene SH2B1, which is involved in the leptin and insulin signaling, have been reported in about 0.5% of children with severe early-onset obesity. These patients show extreme hyperphagia, severe insulin resistance and, in some cases, mild developmental delay.
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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 Socratic graph.