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 (600 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
Specialized connective tissue composed of fat cells (adipocytes). It is the site of stored FATS, usually in the form of triglycerides. In mammals, there are two types of adipose tissue, the white fat and the brown fat. Their relative distributions vary in different species with most adipose tissue being white.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Tissue, Adipose; Fatty Tissue; Tissue, Fatty; Fat Pad; Fat Pads; Pad, Fat; Pads, Fat; Body Fat.
Where it fits in the MeSH classification
- Broader topics
- Connective Tissue
- Narrower topics
- Adipose Tissue, Beige; Adipose Tissue, Brown; Adipose Tissue, White; Epicardial Adipose Tissue
- See also
- Skinfold Thickness; Lipectomy
Related concepts
- Adipocytes
- Triglycerides
- White Fat
- Brown Fat
Research landscape
PubMed indexes 123,122 records tagged with the MeSH heading “Adipose Tissue” (counts retrieved 2026-10-31). 25,371 of them (20.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 41,453 records.
Reviews account for 13,413 records (10.9%) and meta-analyses for 527. Randomized controlled trials number 2,939 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 34,929 |
| 2000-2009 | 21,369 |
| 2010-2019 | 41,453 |
| 2020 onward | 25,371 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 13,413 | 10.9% |
| Meta-analyses | 527 | 0.4% |
| Randomized controlled trials | 2,939 | 2.4% |
Method: PubMed query "Adipose Tissue"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Adipose Tissue Plasticity and Adipogenesis: From Cellular Mechanisms to Therapeutic Targets in Obesity | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 42340603 · DOI · PMC13294325 |
| Adipocyte OX40L promotes adipose T cell activation and insulin resistance in obesity | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42409961 · DOI · PMC13434776 |
| Adipose tissue distribution in metabolic disease: depot-specific biology, clinical assessment, and therapeutic remodeling | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42422426 · DOI · PMC13341497 |
Adipose Tissue Plasticity and Adipogenesis: From Cellular Mechanisms to Therapeutic Targets in Obesity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Purpose of reviewThis review provides an overview of adipose tissue plasticity and adipogenesis as central processes regulating adipose tissue expansion, remodeling, and metabolic function in health and obesity, highlighting their relevance as potential therapeutic targets.
- Closing excerpt
- Targeting adipogenesis and promoting healthy adipose tissue remodeling represent promising strategies for restoring metabolic homeostasis and mitigating obesity-associated diseases.
- 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 (201 words)
Purpose of reviewThis review provides an overview of adipose tissue plasticity and adipogenesis as central processes regulating adipose tissue expansion, remodeling, and metabolic function in health and obesity, highlighting their relevance as potential therapeutic targets.Recent findingsAdipogenesis is a tightly regulated process involving the differentiation of adipose progenitor cells into mature adipocytes through coordinated transcriptional cascades, primarily driven by peroxisome proliferator-activated receptor (PPAR)γ and CCAAT/enhancer-binding protein (C/EBP) family members. This process is further modulated by multiple signaling pathways, including wingless-related integration site (Wnt), bone morphogenetic proteins (BMPs), and insulin signaling, which collectively regulate adipocyte differentiation and metabolic function. Under physiological conditions, the adipose tissue exhibits remarkable plasticity, with adipogenesis supporting lipid buffering capacity and tissue renewal. In obesity, however, chronic nutrient excess and hormonal dysregulation impair this process, favoring adipocyte hypertrophy, hypoxia, and chronic inflammation. These alterations disrupt adipokine secretion and promote ectopic lipid deposition, thereby contributing to metabolic disorders, including insulin resistance and cardiometabolic disease. Adipose tissue plasticity and adipogenesis are critical determinants of metabolic health. Dysregulation of these processes underlies adipose tissue dysfunction and contributes to the development of obesity-related comorbidities. Targeting adipogenesis and promoting healthy adipose tissue remodeling represent promising strategies for restoring metabolic homeostasis and mitigating obesity-associated diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42340603 · DOI · PMC13294325
Adipocyte OX40L promotes adipose T cell activation and insulin resistance in obesity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- T cells contribute critically to obesity-induced adipose inflammation and insulin resistance, yet the co-stimulatory signals that govern their activation in adipose tissue remain unclear.
- Closing excerpt
- Our findings identify adipocyte-derived OX40L as a critical mediator of obesity-associated immune dysfunction and establish it as a targetable checkpoint for tissue-specific immunotherapy in metabolic disease.
- 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 (138 words)
T cells contribute critically to obesity-induced adipose inflammation and insulin resistance, yet the co-stimulatory signals that govern their activation in adipose tissue remain unclear. Here, we systematically profile co-stimulatory molecules in adipocytes and adipose tissue macrophages and identify OX40 ligand (OX40L) as the most robustly upregulated in obesity. OX40L is also elevated in adipocytes from obese humans. Although macrophage-specific OX40L deletion has no metabolic impact, global OX40 deficiency or adipocyte-specific OX40L deletion reduces Th1 cell accumulation in visceral adipose tissue, attenuates inflammation and improves insulin sensitivity without affecting adiposity. These benefits are reversed by Th1 cell transfer. Therapeutic blockade of OX40L with a neutralizing antibody mimics the protective effects of genetic deletion. Our findings identify adipocyte-derived OX40L as a critical mediator of obesity-associated immune dysfunction and establish it as a targetable checkpoint for tissue-specific immunotherapy in metabolic disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42409961 · DOI · PMC13434776
Adipose tissue distribution in metabolic disease: depot-specific biology, clinical assessment, and therapeutic remodeling [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Adipose tissue distribution is a key determinant of metabolic health and cannot be fully explained by total fat mass or body mass index alone.
- Closing excerpt
- This framework highlights the need for standardized depot-specific phenotyping and precision therapies that target metabolically harmful fat distribution rather than total adiposity alone.
- 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 (261 words)
Adipose tissue distribution is a key determinant of metabolic health and cannot be fully explained by total fat mass or body mass index alone. Major adipose compartments, including subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), thermogenic brown and beige adipose tissues, and ectopic lipid accumulation in non-adipose organs, differ markedly in cellular composition, developmental origin, endocrine function, inflammatory status, and metabolic activity. Excess visceral and ectopic fat is strongly associated with insulin resistance, type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), metabolic syndrome (MetS), and organ-specific metabolic injury, whereas lower-body SAT may provide a relatively safe lipid-buffering reservoir. Advances in imaging, body-composition analysis, functional metabolic assessment, single-cell omics, and genetic studies have refined the characterization of adipose tissue distribution and its regulatory basis. Current evidence indicates that regional fat patterning is governed by integrated adipogenic, thermogenic, developmental, endocrine, genetic, and environmental programs, and is further modified by sex, age, ethnicity, diet, physical activity, sleep, and stress. Therapeutic strategies also differ substantially in their effects on adipose distribution. Lifestyle intervention and glucagon-like peptide-1 receptor agonists mainly reduce visceral and ectopic fat alongside overall weight loss, thiazolidinediones (TZDs) more directly reshape lipid partitioning, and thermogenic approaches such as cold exposure and β3-adrenergic stimulation remain biologically attractive but not yet established for routine clinical use. Rather than treating adipose depots as isolated anatomical compartments, this review proposes an integrated framework linking depot-specific biology, lipid-buffering capacity, clinical assessment, and therapeutic remodeling. This framework highlights the need for standardized depot-specific phenotyping and precision therapies that target metabolically harmful fat distribution rather than total adiposity alone.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42422426 · DOI · PMC13341497
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 New genetic loci link adipose and insulin biology to body fat distribution [4]
- Research article Effect of High-Intensity Interval Training on Total, Abdominal and Visceral Fat Mass: A Meta-Analysis [5]
- Research article The effect of exercise on visceral adipose tissue in overweight adults: a systematic review and meta-analysis [6]
- Research article A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat [7]
- Research article An integrated single cell and spatial transcriptomic map of human white adipose tissue [8]
- Research article Epicardial adipose tissue volume assessed by computed tomography and coronary artery disease: a systematic review and meta-analysis [9]
References
- Rocha S, Proença C, Carvalho F, Fernandes E. Adipose Tissue Plasticity and Adipogenesis: From Cellular Mechanisms to Therapeutic Targets in Obesity. . 2026. PMID 42340603 · DOI · PMC13294325
- Song J, Zeng Q, Jiao Y, Sun X, Xie L, Qiu J, et al.. Adipocyte OX40L promotes adipose T cell activation and insulin resistance in obesity. . 2026. PMID 42409961 · DOI · PMC13434776
- LiuLi A, Zhang T, Feng Z. Adipose tissue distribution in metabolic disease: depot-specific biology, clinical assessment, and therapeutic remodeling. . 2026. PMID 42422426 · DOI · PMC13341497
- Shungin D, Winkler TW, Croteau-Chonka DC, Ferreira T, Locke AE, Mägi R, et al.. New genetic loci link adipose and insulin biology to body fat distribution. Nature. 2015. PMID 25673412 · DOI · PMC4338562
- Maillard F, Pereira B, Boisseau N. Effect of High-Intensity Interval Training on Total, Abdominal and Visceral Fat Mass: A Meta-Analysis. Sports Med. 2018. PMID 29127602 · DOI
- Vissers D, Hens W, Taeymans J, Baeyens JP, Poortmans J, Van Gaal L. The effect of exercise on visceral adipose tissue in overweight adults: a systematic review and meta-analysis. PLoS One. 2013. PMID 23409182 · DOI · PMC3568069
- Ismail I, Keating SE, Baker MK, Johnson NA. A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat. Obes Rev. 2012. PMID 21951360 · DOI
- Massier L, Jalkanen J, Elmastas M, Zhong J, Wang T, Nono Nankam PA, et al.. An integrated single cell and spatial transcriptomic map of human white adipose tissue. Nat Commun. 2023. PMID 36922516 · DOI · PMC10017705
- Mancio J, Azevedo D, Saraiva F, Azevedo AI, Pires-Morais G, Leite-Moreira A, et al.. Epicardial adipose tissue volume assessed by computed tomography and coronary artery disease: a systematic review and meta-analysis. Eur Heart J Cardiovasc Imaging. 2018. PMID 29236951 · DOI
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 2026-10-31.
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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.