Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (587 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Body Fat Distribution
Research landscape
PubMed indexes 18,036 records tagged with the MeSH heading “Adiposity” (counts retrieved 2026-10-29). 5,555 of them (30.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 10,831 records.
Reviews account for 1,765 records (9.8%) and meta-analyses for 347. Randomized controlled trials number 912 (5.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 1,801 |
| 2010-2019 | 10,831 |
| 2020 onward | 5,555 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,765 | 9.8% |
| Meta-analyses | 347 | 1.9% |
| Randomized controlled trials | 912 | 5.1% |
Method: PubMed query "Adiposity"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Sex-Specific Differences in Visceral and Subcutaneous Adiposity Accumulation and Their Association With Metabolic Abnormalities | 2025 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41189625 · DOI · PMC12582646 |
| Lifecourse genome-wide association study meta-analysis refines the critical life stages for adiposity's influence on breast cancer risk | 2026 | Meta-analysis Design not recorded in structured metadata | 5 | cc by PMID 41564189 · DOI · PMC12822656 |
| Synergistic associations of metformin and GLP-1 receptor agonist use with adiposity-related cancer incidence in people living with type 2 diabetes | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41178701 · DOI · PMC12803636 |
Sex-Specific Differences in Visceral and Subcutaneous Adiposity Accumulation and Their Association With Metabolic Abnormalities [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Some studies suggest that body fat distribution differs between sexes; there remains a gap regarding the exact mechanisms that regulate these differences and their cardiometabolic consequences.
- Closing excerpt
- In conclusion, within the same mean BMI, males had higher VAT concentrations, whereas in females, despite lower VAT, a worse adverse metabolic profile was observed.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
Some studies suggest that body fat distribution differs between sexes; there remains a gap regarding the exact mechanisms that regulate these differences and their cardiometabolic consequences. This study investigated sex-specific differences influencing the concentration and metabolic risk associated with visceral abdominal adipose tissue (VAT) and subcutaneous adipose tissue (SAT). This cross-sectional study includes outpatients from a university-affiliated public hospital. Consecutive patients aged ≥ 20 years were included in our sample. VAT and SAT were measured using ultrasound (the mean of three attempts). Intra- and interevaluator reproducibility was tested, demonstrating high reliability (> 0.90) for both VAT and SAT. Demographic (age, sex, and self-reported race), anthropometric, behavioral, and biochemical variables were assessed. A total of 253 patients were included. They had a mean age of 46.3 ± 11.6 years (64.4% females and 68.7% non-white). Although the mean total abdominal adipose tissue was similar between sexes (p=0.125), males exhibited a higher mean VAT (7.3 ± 3.0 vs. 6.0 ± 2.1 cm; p p p < 0.05). Among males, VAT did not significantly affect metabolic alterations. In conclusion, within the same mean BMI, males had higher VAT concentrations, whereas in females, despite lower VAT, a worse adverse metabolic profile was observed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41189625 · DOI · PMC12582646
Lifecourse genome-wide association study meta-analysis refines the critical life stages for adiposity's influence on breast cancer risk [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Previous evidence suggests that higher prepubertal adiposity protects against breast cancer risk.
- Closing excerpt
- These findings refine our understanding of adiposity's role in breast cancer and highlight earlier life stages as critical windows for risk modulation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Previous evidence suggests that higher prepubertal adiposity protects against breast cancer risk. Whether this protection extends into early adulthood remains uncertain. We conducted genome-wide association studies on body mass index (BMI) in nulliparous women from menarche to <40 years across five cohorts, with additional analyses in three subintervals of this life stage. Results were meta-analyzed, and two-sample univariable and multivariable Mendelian randomization was applied within a lifecourse framework to assess the effect of BMI on breast cancer risk. Between menarche and <40 years, we observed heterogeneity in genetic effects. Genome-wide correlations further suggest that BMI during this early adult period may be partly influenced by distinct genetic factors compared with adiposity at other life stages. Higher genetically proxied BMI between menarche and 40 years reduced breast cancer risk. This protective effect attenuated after adjusting for prepubertal adiposity. These findings refine our understanding of adiposity's role in breast cancer and highlight earlier life stages as critical windows for risk modulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41564189 · DOI · PMC12822656
Synergistic associations of metformin and GLP-1 receptor agonist use with adiposity-related cancer incidence in people living with type 2 diabetes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundMetformin and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may reduce the risk of adiposity-related cancers in patients with type 2 diabetes (T2D).
- Closing excerpt
- ConclusionIn patients with T2D, dual metformin and GLP-1 RA treatment was associated with a 39% lower incidence of adiposity-related cancers and a 67% lower mortality, with a striking impact on cancer-related outcomes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (230 words)
BackgroundMetformin and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may reduce the risk of adiposity-related cancers in patients with type 2 diabetes (T2D). The potential synergistic effects of these treatments on cancer incidence remain unclear, considering their distinct biological mechanisms and their associated effects on body weight.MethodsA retrospective cohort analysis was conducted using a large global database (TriNetX) of patients with T2D. Three cohorts: single agent use with metformin or GLP-1 RAs, and dual/combination metformin/GLP-1 RA use, were compared with a reference group treated with DPP4 inhibitors (DPP4i). Propensity score matching (1:1) was applied to control for confounders. Cancer incidence and all cause mortality were assessed over 5 years of follow up.ResultsAfter matching, metformin and GLP-1 RA treatment were both associated with a lower risk of all adiposity-related cancers and all-cause mortality; the latter was associated with greater reductions in both. Cancer rates were (hazard ratio) 0.96 [95% CI 0.92, 0.99] and 0.86 [0.82, 0.89], while mortality rates were 0.78 [0.76, 0.80] and 0.61 [0.59, 0.63] for metformin and GLP-1 RA, respectively. Dual therapy showed the strongest association with lower cancer incidence (0.61 [0.57, 0.65]) and mortality (0.33 [0.32, 0.35]). Results were more significant in younger, male patients with obesity.ConclusionIn patients with T2D, dual metformin and GLP-1 RA treatment was associated with a 39% lower incidence of adiposity-related cancers and a 67% lower mortality, with a striking impact on cancer-related outcomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41178701 · DOI · PMC12803636
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Meta-analysis of genome-wide association studies for body fat distribution in 694 649 individuals of European ancestry [4]
- Research article Adiposity and cancer at major anatomical sites: umbrella review of the literature [5]
- Research article Genome-wide association scan meta-analysis identifies three Loci influencing adiposity and fat distribution [6]
- Research article Leptin, Obesity, and Leptin Resistance: Where Are We 25 Years Later? [7]
- Research article Sex Differences in Body Composition [8]
- Research article Rapid weight gain during infancy and subsequent adiposity: a systematic review and meta-analysis of evidence [9]
References
- Rodrigues IG, Arcoverde GMPF, do Nascimento CLC, Ferraz VD, da Silva NF, de Arruda IKG, et al.. Sex-Specific Differences in Visceral and Subcutaneous Adiposity Accumulation and Their Association With Metabolic Abnormalities. . 2025. PMID 41189625 · DOI · PMC12582646
- Power GM, Bhatta L, Hughes AM, Medina-Gomez C, Richmond A, Leyden G, et al.. Lifecourse genome-wide association study meta-analysis refines the critical life stages for adiposity's influence on breast cancer risk. . 2026. PMID 41564189 · DOI · PMC12822656
- Henney AE, Heague M, Riley DR, Hydes TJ, Anson M, Alam U, et al.. Synergistic associations of metformin and GLP-1 receptor agonist use with adiposity-related cancer incidence in people living with type 2 diabetes. . 2026. PMID 41178701 · DOI · PMC12803636
- Pulit SL, Stoneman C, Morris AP, Wood AR, Glastonbury CA, Tyrrell J, et al.. Meta-analysis of genome-wide association studies for body fat distribution in 694 649 individuals of European ancestry. Hum Mol Genet. 2019. PMID 30239722 · DOI · PMC6298238
- Kyrgiou M, Kalliala I, Markozannes G, Gunter MJ, Paraskevaidis E, Gabra H, et al.. Adiposity and cancer at major anatomical sites: umbrella review of the literature. BMJ. 2017. PMID 28246088 · DOI · PMC5421437
- Lindgren CM, Heid IM, Randall JC, Lamina C, Steinthorsdottir V, Qi L, et al.. Genome-wide association scan meta-analysis identifies three Loci influencing adiposity and fat distribution. PLoS Genet. 2009. PMID 19557161 · DOI · PMC2695778
- Izquierdo AG, Crujeiras AB, Casanueva FF, Carreira MC. Leptin, Obesity, and Leptin Resistance: Where Are We 25 Years Later?. Nutrients. 2019. PMID 31717265 · DOI · PMC6893721
- Bredella MA. Sex Differences in Body Composition. Adv Exp Med Biol. 2017. PMID 29224088 · DOI
- Zheng M, Lamb KE, Grimes C, Laws R, Bolton K, Ong KK, et al.. Rapid weight gain during infancy and subsequent adiposity: a systematic review and meta-analysis of evidence. Obes Rev. 2018. PMID 29052309 · DOI · PMC6203317
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.