ReviewJournal of internal medicine2018
Genes that make you fat, but keep you healthy.
Review in Journal of internal medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Adipose Tissue Epigenetic Profile in Obesity-Related Dysglycemia - A Systematic Review.Frontiers in endocrinology · 2021Pooled it
- Genetic subtyping of obesity reveals biological insights into the uncoupling of adiposity from its cardiometabolic comorbidities.Nature medicine · 2025Article
- Exploring the genetic intersection between obesity-associated genetic variants and insulin sensitivity indices.Scientific reports · 2025Article
- Article
- Sex differences in the relationship between body composition and MASLD progression in a murine model of metabolic syndrome.iScience · 2025Article
- Using clustering of genetic variants in Mendelian randomization to interrogate the causal pathways underlying multimorbidity from a common risk factor.Genetic epidemiology · 2025Article
- Tissue-specific genetic variation suggests distinct molecular pathways between body shape phenotypes and colorectal cancer.Science advances · 2024Article
- Fat as a Friend or Foe of the Bone.Current osteoporosis reports · 2024Review
- Heterogeneously elevated branched-chain/aromatic amino acids among new-onset type-2 diabetes mellitus patients are potentially skewed diabetes predictors.World journal of diabetes · 2024Article
- Defining type 2 diabetes polygenic risk scores through colocalization and network-based clustering of metabolic trait genetic associations.Genome medicine · 2024Article
- MAFLD: an ideal framework for understanding disease phenotype in individuals of normal weight.Therapeutic advances in endocrinology and metabolism · 2024Review
- Relevance of body composition in phenotyping the obesities.Reviews in endocrine & metabolic disorders · 2023Review
- Body composition and mortality from middle to old age: a prospective cohort study from the UK Biobank.International journal of obesity (2005) · 2023Article
- Article
- A non-coding variant linked to metabolic obesity with normal weight affects actin remodelling in subcutaneous adipocytes.Nature metabolism · 2023Article
- A phenome-wide comparative analysis of genetic discordance between obesity and type 2 diabetes.Nature metabolism · 2023Article
- Disentangling the aetiological pathways between body mass index and site-specific cancer risk using tissue-partitioned Mendelian randomisation.British journal of cancer · 2023Article
- Metabolic (dysfunction)-associated fatty liver disease in individuals of normal weight.Nature reviews. Gastroenterology & hepatology · 2022Review
- Effects of general and central adiposity on circulating lipoprotein, lipid, and metabolite levels in UK Biobank: A multivariable Mendelian randomization study.The Lancet regional health. Europe · 2022Article
- Inherited basis of visceral, abdominal subcutaneous and gluteofemoral fat depots.Nature communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Obesity prevalence continues to rise worldwide, posing a substantial burden on people's health. However, up to 45% of obese individuals do not suffer from cardiometabolic complications, also called the metabolically healthy obese (MHO). Concurrently, up to 30% of normal-weight individuals demonstrate cardiometabolic risk factors that are generally observed in obese individuals, the metabolically obese normal weight (MONW). Besides lifestyle, environmental factors and demographic factors, innate biological mechanisms are known to contribute to the aetiology of the MHO and MONW phenotypes, as well. Experimental studies in animal models have shown that adipose tissue expandability, fat distribution, adipogenesis, adipose tissue vascularization, inflammation and fibrosis, and mitochondrial function are the main mechanisms that uncouple adiposity from its cardiometabolic comorbidities. We reviewed current genetic association studies to expand insights into the biology of MHO/MONW phenotypes. At least four genetic loci were identified through genome-wide association studies for body fat percentage (BF%) of which the BF%-increasing allele was associated with a protective effect on glycemic and lipid outcomes. For some, this association was mediated through favourable effects on body fat distribution. Other studies that characterized the genetic susceptibility of insulin resistance found that a higher susceptibility was associated with lower overall adiposity due to less fat accumulation at hips and legs, suggesting that an impaired capacity to store fat subcutaneously or a preferential storage in the intra-abdominal cavity may be metabolically harmful. Clearly, more work remains to be done in this field, first through gene discovery and subsequently through functional follow-up of identified genes.
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.