ReviewEuropean child & adolescent psychiatry2010
From monogenic to polygenic obesity: recent advances.
Review in European child & adolescent psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.
- Polygenic Risk and Nutrient Intake Interactions on Obesity Outcomes: A Systematic Review and Meta-Analysis of Observational Studies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Pooled it
- Associations between polygenic risk for obesity, body mass index and cognitive performance: Age as moderating factor.Brain, behavior, & immunity - health · 2026Article
- Article
- NovelInternational journal of molecular sciences · 2026Article
- Genetic architecture of obesity and advances in precision pharmacotherapy: a comprehensive review.Acta biochimica Polonica · 2026Review
- Six Years of Genetic Diagnosis of Severe Early-Onset Obesity in a French Cohort.Obesity science & practice · 2025Article
- Nutrigenomics of Obesity: Integrating Genomics, Epigenetics, and Diet-Microbiome Interactions for Precision Nutrition.Life (Basel, Switzerland) · 2025Review
- Obesity genetic association prospective cohort utilizing single center real-world evidence data.Medicine · 2025Article
- Widespread recessive effects on common diseases in a cohort of 44,000 British Pakistanis and Bangladeshis with high autozygosity.American journal of human genetics · 2025Article
- Article
- Integrating Genetic Insights, Technological Advancements, Screening, and Personalized Pharmacological Interventions in Childhood Obesity.Advances in therapy · 2025Review
- Navigating Cardiovascular Challenges of Obesity: Exploring Preventive Approaches.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Article
- Refining the scope of genetic influences on alcohol misuse through environmental stratification and gene-environment interaction.Alcohol, clinical & experimental research · 2024Article
- Review
- Whole genome sequencing of mouse lines divergently selected for fatness (FLI) and leanness (FHI) revealed several genetic variants as candidates for novel obesity genes.Genes & genomics · 2024Article
- The melanocortin-4 receptor pathway and the emergence of precision medicine in obesity management.Diabetes, obesity & metabolism · 2024Article
- Precision Nutrition and Cardiovascular Disease Risk Reduction: the Promise of High-Density Lipoproteins.Current atherosclerosis reports · 2023Review
- Assessing efficiency of fine-mapping obesity-associated variants through leveraging ancestry architecture and functional annotation using PAGE and UKBB cohorts.Human genetics · 2023Article
- Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heritability of obesity and body weight in general is high. A small number of confirmed monogenic forms of obesity-the respective mutations are sufficient by themselves to cause the condition in food abundant societies-have been identified by molecular genetic studies. The elucidation of these genes, mostly based on animal and family studies, has led to the identification of important pathways to the disorder and thus to a deeper understanding of the regulation of body weight. The identification of inborn deficiency of the mostly adipocyte-derived satiety hormone leptin in extremely obese children from consanguineous families paved the way to the first pharmacological therapy for obesity based on a molecular genetic finding. The genetic predisposition to obesity for most individuals, however, has a polygenic basis. A polygenic variant by itself has a small effect on the phenotype; only in combination with other predisposing variants does a sizeable phenotypic effect arise. Common variants in the first intron of the 'fat mass and obesity associated' gene (FTO) result in an elevated body mass index (BMI) equivalent to approximately +0.4 kg/m(2) per risk allele. The FTO variants were originally detected in a genome wide association study (GWAS) pertaining to type 2 diabetes mellitus. Large meta-analyses of GWAS have subsequently identified additional polygenic variants. Up to December 2009, polygenic variants have been confirmed in a total of 17 independent genomic regions. Further study of genetic effects on human body weight regulation should detect variants that will explain a larger proportion of the heritability. The development of new strategies for diagnosis, treatment and prevention of obesity can be anticipated.
Indexed as
Identifiers
What OpenQuestion holds
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.