NYU Abu Dhabi scientists reveal a hidden biological switch linked to obesity

Samira Khalaji, Research Associate at the Center for Genomics and Systems Biology

Not all fat cells grow the same, and that difference may be shaping your health

ABU DHABI, UNITED ARAB EMIRATES, March 10, 2026 /EINPresswire.com/ --

Not all fat tissue behaves in the same way. Two people can have a similar body weight but very different metabolic health, prompting scientists to ask what helps fat tissue grow and function in a more adaptive way.

A new study from researchers at New York University Abu Dhabi (NYUAD), together with collaborators, published recently in Cell Death & Disease journal by Springer Nature, investigated this question. The study identifies an important role for a protein called nuclear myosin 1 (NM1) in supporting the gene activity and metabolic balance needed for normal fat cell development and fat tissue health.

Fat tissue is more than a storage site for excess energy. It also acts as an endocrine organ, releasing signals that influence metabolism throughout the body. When fat tissue expands in a healthier and more adaptive way, it can help the body manage excess energy more effectively. When this process becomes dysregulated, fat tissue may function less efficiently and become more prone to inflammation and metabolic imbalance.

In the study, the researchers focused on NM1, a protein that works inside the cell nucleus, where it helps regulate how DNA is packaged and accessed. This process influences which genes are turned on or off as cells change from one state to another.

In mouse studies, the team found that loss of NM1 disrupted gene programs involved in fat cell formation and mitochondrial function, which is essential for cellular energy balance. As a result, stem cells were less able to develop into mature fat cells. The researchers followed mice without NM1 as they aged and found that they gradually accumulated more visceral fat, the fat around internal organs. They also saw signs that the fat tissue was functioning less well, with lower activity in genes involved in healthy fat cell development and energy use, and higher activity in genes linked to inflammation. This suggests that NM1 helps fat tissue develop and function properly.

The team also compared their results with human data and found signs that similar biological processes may be at work in both mice and humans. However, further studies in human fat tissue will be needed to confirm exactly how this process works in the body.

As the study suggests, problems in fat tissue may begin at the level of gene organization inside cells, long before disease symptoms appear.

Hence, rather than viewing obesity as a sole result of lifestyle choices, this research highlights the importance of cellular and genetic regulation. These findings shift the focus from the mere amount of fat present to the body’s ability to form and adapt healthy fat tissue.

Focusing on fat tissue formation and flexibility, rather than just quantity, opens new paths for research into metabolic disease prevention, screening, and treatment.

“These findings show that obesity and metabolic disease are not only about diet, exercise, or calories. They also depend on how well fat tissue develops and adapts at the genome level. In mice, NM1 helps fat cells form and function properly. When NM1 is missing, fat tissue changes in unhealthy ways and shows more signs of inflammation over time. This suggests that early changes in how genes are controlled inside cells may play an important role in metabolic disease,” says Samira Khalaji, Research Associate at the Center for Genomics and Systems Biology.

DOI: https://doi.org/10.1038/s41419-026-08525-3

Enas Qudeimat
NYUAD CGSB
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