Researchers at NYU Abu Dhabi, working with colleagues in the Czech Republic and France, have shown that mice missing a protein called Nuclear Myosin 1 (NM1) gain weight steadily as they age — even when they eat the same amount of food as normal mice. By 12 months, the NM1-deficient mice were on average 35% heavier, with their share of belly fat to body weight more than double that of healthy animals.
The findings, published in Cell Death and Disease, point to a previously hidden layer of obesity biology: how fat cells fold and read their own DNA.
A Motor Inside the Nucleus
Motor proteins are best known for using energy to create movement within cells and muscles. But the motor protein NM1 has a different function: it lives inside the cell nucleus, where it helps unwind DNA so that genes can be switched on at the right time. Think of it as a librarian who decides which books — which genes — are pulled off the shelf on any given day.
The study’s researchers, Samira Khalaji (lead author) and Piergiorgio Percipalle (group leader), wanted to know what happens when stem cells — the precursors to fat cells — lose access to that librarian. Without NM1, mouse stem cells struggled to mature into proper fat cells. Instead of producing many small, healthy fat cells, the tissue produced fewer, oversized ones — a pattern doctors call hypertrophy. Hypertrophic fat is the kind most strongly linked to inflammation, insulin resistance and type 2 diabetes in people.
Eating the Same, But Getting Fatter
To rule out the obvious explanation, the team measured how much the mice ate. The NM1-deficient mice did not eat more, yet they grew heavier year on year. Their fat accumulated around the abdomen — the same visceral fat tied to the most serious metabolic diseases in humans, such as obesity and type 2 diabetes.
“The fat tissue looked metabolically sick.” – Enas Qudeimat
When the researchers looked inside the fat tissue itself, they found a cascade of disturbances. Genes that normally drive healthy fat-cell development were switched off. Inflammatory signals were active, including two markers well known in obesity research (TNF and interferon-gamma). Mitochondria — the cellular power plants that burn fat for energy — were malfunctioning. In short, the fat tissue looked metabolically sick.
Why This Matters for Humans
Mouse studies do not always translate into similar findings in humans, so the team checked whether the same regulatory wiring exists in people. Using human genetic data, they identified a network of genetic variants around MYO1C — the human equivalent of NM1 — that shape how fat tissue behaves. Three variants stood out as particularly important, and all three had previously been linked to body weight and metabolic traits.
“Small differences in how a single nuclear motor works could help explain why some people accumulate visceral fat more readily than others.” – Enas Qudeimat
That cross-species overlap is the part most worth paying attention to. It suggests that small differences in how a single nuclear motor works could help explain why some people accumulate visceral fat more readily than others, independent of what they eat.
Not a Treatment, But a New Lens
As the authors make very clear, this study does not mean we have found a cure for obesity. This research was conducted in mice, and the correlational findings in humans need to be studied further. We do not yet know whether boosting NM1 activity would help patients, or how much of human obesity risk these variants explain.
What the study does offer is a new lens. Over time, obesity has been framed first as a calorie problem, then as a hormone problem, and most recently as a gut microbiome problem. This work adds another layer: how the three-dimensional architecture of DNA inside fat cells helps to shape their long-term health.
Read this article to learn more about the links between our food, gut microbiome, and human health!
Diet Still Matters — But Cells Might Too
The practical advice for people mindful of their health remains the same: diet, movement and sleep still matter. But for researchers, this study opens a fresh line of inquiry — one that could eventually help identify who is biologically more vulnerable to visceral fat gain, and design treatments that work at the level of the nucleus itself.
It seems the fight against obesity may be waged not only in the kitchen, but also in the cell.
Article based on Khalaji et al., Cell Death and Disease (2026).
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