Visceral fat, which surrounds organs deep in the abdomen, was more strongly associated with type 2 diabetes risk than body mass index (BMI) in a study of 36,831 UK Biobank participants published July 15, 2026, in the International Journal of Obesity. A second study, published online July 26 in Adipocyte, compared visceral and subcutaneous fat from 22 patients with obesity and found distinct cellular behaviors that may help explain why fat location matters for metabolic health.
Visceral and subcutaneous fat occupy different locations
Subcutaneous adipose tissue (SAT) is stored directly beneath the skin, including around the abdomen, hips and thighs. Visceral adipose tissue (VAT) is located deeper in the abdominal cavity, around internal organs. Both are biologically active tissues rather than passive storage spaces. Fat cells store and release fatty acids and respond to insulin and other hormonal signals. Their surrounding blood vessels, immune cells and extracellular matrix also influence how the tissue grows and functions.
This distinction matters because two people with the same BMI can have substantially different distributions of visceral, subcutaneous and organ-associated fat. BMI is calculated from body weight and height. It does not distinguish fat mass from muscle or identify fat stored around the abdominal organs. Research into the relationship between metabolism and aging has similarly emphasized that metabolic risk cannot always be inferred from weight alone.
Visceral fat increased with age even when BMI was similar
Rask-Andersen and colleagues analyzed magnetic resonance imaging (MRI) measurements from 36,831 white British adults aged 45 to 82 years in the UK Biobank. Of these, 1,688 had repeated imaging, with a mean interval of 2.7 years. The team examined nine imaging-derived traits, including visceral and subcutaneous fat, pancreatic and liver measures, and fat infiltration in thigh muscle. They linked those measurements with subsequent type 2 diabetes, abnormal blood lipids, hypertension, heart attack and cerebral infarction.
At the first scan, the average age was 63.9 years. Older participants generally had more visceral fat and greater fat infiltration in the pancreas and thigh muscles, even where BMI was similar. The repeat-imaging subgroup supported a pattern of increasing metabolically unfavorable fat depots over time. That does not mean every individual’s visceral fat rises steadily with age, but it suggests that BMI can obscure shifts in body composition.
Across the evaluated outcomes, visceral fat showed a particularly strong association with type 2 diabetes. The researchers also used Mendelian randomization, a genetic epidemiology method intended to probe possible causal relationships, to examine the patterns from a different angle. They found support for a contribution of visceral fat to diabetes risk beyond BMI. The genetic analyses strengthen the investigation but do not replace randomized intervention evidence.
The results were more selective than a broad claim that visceral fat independently predicted every cardiovascular outcome. After correction for multiple testing and adjustment for BMI, significant associations remained principally for type 2 diabetes and hyperlipidemia. The analyses did not establish equally robust BMI-independent associations for heart attack or cerebral infarction. This distinction is important when interpreting the study’s cardiometabolic implications.
Fat cells from different depots behaved differently in laboratory tests
A separate investigation published in Adipocyte compared paired visceral and subcutaneous abdominal fat samples from 22 patients with obesity undergoing elective Roux-en-Y gastric bypass surgery. Researchers examined fat-cell diameter, gene expression, glucose uptake, glycerol release as a measure of lipolysis, and proteins involved in tissue structure.
Subcutaneous fat cells were larger on average and showed higher basal lipolysis and expression of genes associated with fat breakdown. By contrast, visceral adipocytes showed greater stimulated lipolytic responsiveness, as well as higher basal and insulin-stimulated glucose uptake in the isolated-cell assays. These findings complicate any simple assertion that individual visceral fat cells are uniformly less responsive to insulin or metabolically inactive.
Subcutaneous tissue also had higher levels of certain extracellular matrix components linked to tissue flexibility and more caveolin-1 protein in its adipocytes. The investigators proposed that these characteristics could support a greater capacity for subcutaneous fat expansion. They additionally identified an association between expression of the collagen gene COL3A1 in subcutaneous fat and measures including BMI, fat-cell size and insulin resistance. Those associations do not establish that COL3A1 itself causes insulin resistance.
The study’s 22 surgical patients are a highly selected group. Its isolated-cell measurements cannot be read as direct evidence that one entire fat depot is harmless or that laboratory glucose uptake predicts long-term disease outcomes. Rather, the work highlights the different regulatory environments of two fat stores.
Subcutaneous fat may provide a safer storage site until its capacity is exceeded
One explanation for the different clinical associations involves the capacity of subcutaneous adipose tissue to accommodate excess energy. When fat can be stored and remodeled in subcutaneous depots, less may accumulate in organs and other tissues that are poorly suited to storing large quantities of lipid. When those storage and remodeling processes become constrained, excess fatty acids may contribute to fat accumulation in the liver, pancreas and skeletal muscle.
Visceral fat also sits in close physiological communication with the liver through its venous drainage and secretion of signaling molecules. Greater visceral fat often accompanies inflammatory signaling and insulin resistance. These pathways help explain the plausibility of the epidemiologic findings, but neither 2026 paper established a complete sequence proving that visceral fat alone caused diabetes in individual participants.
That broader metabolic context also helps explain why changes in lean mass during obesity treatment deserve attention and why obesity-related health risks cannot be reduced to one number on a scale.
Waist circumference is informative but cannot measure visceral fat directly
Clinical assessment often uses waist circumference alongside BMI, blood pressure, blood glucose and lipid measurements because abdominal size can provide additional information about cardiometabolic risk. Yet waist circumference cannot distinguish visceral from subcutaneous abdominal fat. MRI can quantify these compartments more directly, but its cost and availability make routine scanning impractical for most people.
The UK Biobank authors emphasized the need for more scalable measurements or biomarkers that reflect fat distribution and ectopic fat. The new findings do not establish a reason for healthy adults to request an MRI solely to measure visceral fat. They also do not supply a validated numerical target for visceral fat volume or prove that a particular diet, medication or exercise routine selectively reduces the disease risk associated with VAT.
What the evidence cannot yet answer
The July study was primarily observational, despite its genetic analyses. Participants were white British adults aged 45 to 82, and those undergoing imaging tended to be healthier than the wider UK Biobank cohort. The repeat-imaging sample was much smaller than the total sample. Residual confounding and limitations of genetic assumptions remain possible, and the findings may not generalize equally to younger or more diverse populations.
The Adipocyte study had just 22 participants undergoing bariatric surgery, and its detailed tissue assays were not designed to estimate future cardiovascular or diabetes events. Although its biology is informative, cell behavior measured outside the body must not be equated with whole-body metabolic risk.
Funding for the UK Biobank analysis included Swedish research organizations and the Novo Nordisk Foundation; its authors declared no competing interests. Both studies add evidence that fat distribution and tissue biology matter. Neither demonstrates that all subcutaneous fat is protective or that visceral fat is the sole determinant of metabolic disease.
References
- Rask-Andersen M, Lo Faro V, Karlsson T, Johansson Å. Age-related changes in adiposity and cardiometabolic disease risk: a longitudinal and prospective study in the UK Biobank. International Journal of Obesity. 2026. DOI: 10.1038/s41366-026-02168-2.
- Depot-specific differences in visceral and subcutaneous adipose tissue from patients with obesity. Adipocyte. 2026;15(1):2708374. DOI: 10.1080/21623945.2026.2708374.