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 (716 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
Fatty tissue in the region of the abdomen. It includes the abdominal subcutaneous fat and the intra-abdominal fat.
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: Abdominal Fats; Fats, Abdominal; Abdominal Adipose Tissue; Adipose Tissue, Abdominal; Fat, Abdominal.
Where it fits in the MeSH classification
- Broader topics
- Adipose Tissue, White
- Narrower topics
- Intra-Abdominal Fat; Subcutaneous Fat, Abdominal
- See also
- Obesity, Abdominal
Related concepts
- Abdomen
- Abdominal Subcutaneous Fat
- Intra-Abdominal Fat
Research landscape
PubMed indexes 11,771 records tagged with the MeSH heading “Abdominal Fat” (counts retrieved 2026-10-31). 3,464 of them (29.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 6,493 records.
Reviews account for 791 records (6.7%) and meta-analyses for 112. Randomized controlled trials number 651 (5.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 2,028 |
| 2010-2019 | 6,493 |
| 2020 onward | 3,464 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 791 | 6.7% |
| Meta-analyses | 112 | 1.0% |
| Randomized controlled trials | 651 | 5.5% |
Method: PubMed query "Abdominal Fat"[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 |
|---|---|---|---|---|
| Low Visceral Adipose Tissue Predicts the Outcome of Neoadjuvant Chemotherapy for Colorectal Liver Metastases: A Multicentre Real-World Study | 2025 | Research article Design not recorded in structured metadata | 20 | cc by PMID 40170387 · DOI · PMC11961552 |
| Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation | 2026 | Research article Design not recorded in structured metadata | 15 | cc by PMID 41680163 · DOI · PMC12902017 |
| Blocking the SIRPα-CD47 axis promotes macrophage phagocytosis of exosomes derived from visceral adipose tissue and improves inflammation and metabolism in mice | 2025 | Research article Design not recorded in structured metadata | 15 | cc by PMID 40016734 · DOI · PMC11869713 |
Low Visceral Adipose Tissue Predicts the Outcome of Neoadjuvant Chemotherapy for Colorectal Liver Metastases: A Multicentre Real-World Study [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundVisceral obesity (VO), associated with excessive visceral adipose tissue (VAT), has been extensively studied in cancer.
- Closing excerpt
- Baseline VAT and ΔVAT may serve as important indicators for risk stratification and personalized treatment in CRLM patients.
- 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 (179 words)
BackgroundVisceral obesity (VO), associated with excessive visceral adipose tissue (VAT), has been extensively studied in cancer. However, whether low VAT can predict the prognosis of colorectal liver metastases (CRLM) undergoing neoadjuvant chemotherapy (NAC) remains unknown.MethodsThis multicentre real-world cohort study analysed data from initially resectable CRLM patients who received NAC. The predictive effect of VAT on progression-free survival (PFS) and overall survival (OS) was evaluated using restricted cubic splines (RCS). VAT was categorized into low/normal VAT and VO groups using X-tile. The prognostic differences were further assessed through Kaplan-Meier (KM) analysis. The impact of changes in VAT (ΔVAT) after NAC was evaluated.ResultsAmong 1524 CRLM patients, 1105 patients (72.51%) were under 65 years old, with a median VAT of 84.00 (36.24-148.00) cm2. Of all patients, 804 (52.76%) were female. A U-shaped nonlinear relationship was observed between VAT and both PFS/OS (p ConclusionsThis study is the first to reveal that low VAT and VO can predict PFS and OS in CRLM patients undergoing NAC. Baseline VAT and ΔVAT may serve as important indicators for risk stratification and personalized treatment in CRLM patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40170387 · DOI · PMC11961552
Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- How cellular metabolism facilitates tissue-resident macrophage maintenance remains elusive.
- Closing excerpt
- Our data thus reveal an unexpected function of SerpinB2 in the regulation of mitochondrial function and survival of tissue-resident macrophages.
- 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 (189 words)
How cellular metabolism facilitates tissue-resident macrophage maintenance remains elusive. Here we show that visceral adipose tissue (VAT)-resident macrophages, unlike monocyte-derived macrophages, are enriched with mitochondrial-specific antioxidant enzymes restraining inflammation and promoting VAT homeostasis and insulin sensitivity. Additionally, VAT resident macrophages express high levels of plasminogen activator inhibitor type 2, encoded by SerpinB2, which is involved in the blood coagulation cascade. SerpinB2 promotes adipose resident macrophage survival by regulating mitochondrial oxidative phosphorylation and preventing the release of pro-apoptotic cytochrome c from the mitochondria into the cytoplasm via antioxidant glutathione production. Chronic inflammation, such as obesity, diminishes SerpinB2 expression in VAT macrophages in patients and mice, leading to the decline of this macrophage subset. Mechanistically, interferon-γ elevation in diabetes induces Ikaros, a transcriptional suppressor, which binds to the SerpinB2 promoter and decreases SerpinB2 expression. Congruently, selective depletion of the IFN-γ receptor in myeloid cells or supplementation of macrophage-specific SerpinB2 deficient mice with N-acetylcysteine, a glutathione precursor, restores VAT resident macrophage survival, decreases adipocyte size, and improves glucose tolerance and insulin sensitivity. Our data thus reveal an unexpected function of SerpinB2 in the regulation of mitochondrial function and survival of tissue-resident macrophages.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41680163 · DOI · PMC12902017
Blocking the SIRPα-CD47 axis promotes macrophage phagocytosis of exosomes derived from visceral adipose tissue and improves inflammation and metabolism in mice [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAdipose tissue plays a pivotal role in systemic metabolism and maintaining bodily homeostasis.
- Closing excerpt
- The SIRPα-CD47 axis emerges as a potential therapeutic target for obesity and its associated complications.
- 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 (348 words)
BackgroundAdipose tissue plays a pivotal role in systemic metabolism and maintaining bodily homeostasis. Exosomes from adipose tissues, known as AT-Exos, are recognized as important messengers in the communication between adipose tissue and other organs. Despite this, the alterations in exosome composition and the functional disparities among depot-specific AT-Exos in obesity remain elusive.MethodsIn this work, we utilized lipidomics and microRNA (miRNA) sequencing to elucidate the lipid and miRNA profiles of AT-Exos in a diet-induced obesity model. We identified obesity-related miRNAs in AT-Exos and further explored their mechanisms using gain- and loss-of-function experiments. To evaluate the metabolic effects of AT-Exos on adipocytes, we conducted RNA-sequencing (RNA-seq) and confirmed our findings through Quantitative Real-time PCR (qPCR) and Western bolt analyses. Meanwhile, a mouse model with intraperitoneal injections was utilized to validate the role of exosomes derived from visceral white adipose tissue (vWAT-Exos) in obesity progression in vivo. Finally, we explored potential therapeutic intervention strategies targeting AT-Exos, particularly focusing on modulating the SIRPα-CD47 axis to enhance macrophage phagocytosis using Leptin-deficient (ob/ob) mice and SIRPα knock-out mice.ResultsOur study revealed that obesity-related metabolism affects the biological processes of AT-Exos, with depot-specific secretion patterns. In obesity, the lipidome profile of AT-Exos was significantly altered, and diet can modify the miRNA content and function within these exosomes, influencing lipid metabolism and inflammatory pathways that contribute to metabolic dysregulation. Specifically, we identified that miR-200a-3p and miR-200b-3p promoted lipid accumulation in 3T3L1 cells partly through the PI3K/AKT/mTOR pathway. RNA-Seq analysis revealed that AT-Exos from different fat depots exerted distinct effects on adipocyte metabolism, with obese vWAT-Exos being notably potent in triggering inflammation and lipid accumulation in diet-induced obesity. Additionally, we found that inhibiting the SIRPα-CD47 axis can mitigate metabolic disorders induced by obese vWAT-Exos or ob/ob mice, partly due to the enhanced clearance of vWAT-Exos. Consistent with this, SIRPα-deficient mice exhibited a reduction in vWAT-Exos and displayed greater resistance to obesity.ConclusionsThis study elucidates that diet-induced obesity altered the lipid and miRNA profiles of AT-Exos, which involved in modulating adipocyte inflammation and metabolic balance. The SIRPα-CD47 axis emerges as a potential therapeutic target for obesity and its associated complications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40016734 · DOI · PMC11869713
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 Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity [4]
- Research article Pathophysiology of human visceral obesity: an update [5]
- Research article Subcutaneous and visceral adipose tissue: structural and functional differences [6]
- Research article Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement [7]
- Research article Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk [8]
- Research article The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis [9]
References
- Chen Y, Jia H, Ye R, Zhou Z, Chen W, Zheng M, et al.. Low Visceral Adipose Tissue Predicts the Outcome of Neoadjuvant Chemotherapy for Colorectal Liver Metastases: A Multicentre Real-World Study. . 2025. PMID 40170387 · DOI · PMC11961552
- Vasamsetti SB, Sadaf S, Uddin MA, Shen J, Johny E, Mondal A, et al.. Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation. . 2026. PMID 41680163 · DOI · PMC12902017
- Lin YK, Pan YF, Jiang TY, Chen YB, Shang TY, Xu MY, et al.. Blocking the SIRPα-CD47 axis promotes macrophage phagocytosis of exosomes derived from visceral adipose tissue and improves inflammation and metabolism in mice. . 2025. PMID 40016734 · DOI · PMC11869713
- Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al.. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009. PMID 19805654 · DOI
- Tchernof A, Després JP. Pathophysiology of human visceral obesity: an update. Physiol Rev. 2013. PMID 23303913 · DOI
- Ibrahim MM. Subcutaneous and visceral adipose tissue: structural and functional differences. Obes Rev. 2010. PMID 19656312 · DOI
- Neeland IJ, Ross R, Després JP, Matsuzawa Y, Yamashita S, Shai I, et al.. Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement. Lancet Diabetes Endocrinol. 2019. PMID 31301983 · DOI
- Després JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E, et al.. Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. Arterioscler Thromb Vasc Biol. 2008. PMID 18356555 · DOI
- Shuster A, Patlas M, Pinthus JH, Mourtzakis M. The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis. Br J Radiol. 2012. PMID 21937614 · DOI · PMC3473928
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.