Dr Yvonne Böttcher | How Different Types of Fat Shape Health and Disease

In their recent study, with Sadia Saeed and Lars la Cour Poulsen as lead researchers, the team analysed paired samples of both fat types taken from people with obesity. They used advanced genetic tools that allow scientists to see which parts of the genome are “open for business” – in other words, regions where genes are more likely to be switched on.

The team found clear and consistent differences between the two fat depots. Visceral fat showed roughly twice as many uniquely open regions in the genome compared with subcutaneous fat. This matters, because open regions often show higher gene activity. The finding suggests that visceral fat may be more dynamically regulated – and potentially more reactive in ways that influence disease risk.

The researchers also discovered that some of the more open regions in subcutaneous fat showed stronger links to tissue structure and metabolic processes.

Visceral fat, however, showed greater activity near genes associated with heart and metabolic disease pathways. This may help explain why fat stored around the organs is more strongly tied to poor health outcomes.

In a second related study, the researchers focused on another layer of gene regulation: chemical tags on RNA molecules. RNA carries the instructions that cells use to build proteins, and small chemical marks can influence how long those instructions last and how efficiently they are used.

Böttcher’s team with Torunn Rønningen as lead researcher mapped a common RNA modification called m6A across both fat depots. They identified hundreds of genes that showed depot-specific patterns of this chemical tagging. Some differences were also linked to obesity itself. In addition, the researchers observed that many signals seem to origin from non-fat cells, with a higher amount of such signals in visceral fat.

This points towards a contribution of other cell types, such as immune cells, that may influence obesity associated complications.

Early functional experiments suggested these RNA marks can affect how long specific RNA messages survive inside cells. That means they may play a role in fine-tuning how fat tissue functions over time.

Crucially, in both studies, these molecular patterns were not just abstract lab findings. The scientists found that specific gene activity patterns and modifications in each fat depot were linked to real-world clinical measures, including insulin levels, blood sugar and blood lipids. This strengthens the case that the biology of fat location genuinely affects metabolic health.

Taken together, the work by Böttcher and colleagues paints a much richer picture of body fat than the simple idea of “too much fat”. It shows that fat depots differ at multiple layers of biological control – from DNA accessibility to RNA chemistry – and that these differences are connected to metabolic health.

Although the research is still developing, it offers an important step toward more precise obesity science. By understanding why fat depots behave differently, scientists may eventually be better equipped to predict risk, personalise treatments and design more targeted interventions.