Daijiworld Media Network - Abu Dhabi
Abu Dhabi, May 9: Scientists at New York University Abu Dhabi have discovered a protein that plays a central role in regulating fat tissue health, potentially reshaping how obesity is understood and treated.
The research identifies a protein called nuclear myosin 1c (NM1) as a “master regulator” of gene activity inside fat cells. According to the study, NM1 helps control how genes switch on and off within the cell nucleus, ensuring that fat tissue develops and functions normally.
When this protein is missing or does not function correctly, fat cells fail to mature properly. Instead of developing into healthy cells, they become abnormally large and accumulate excessive amounts of lipids.
Researchers found that these enlarged fat cells can spread across the body, not just in common areas like the abdomen or shoulders, but also around vital organs such as the liver—raising concerns about links to more serious metabolic diseases.
The study also observed that this condition is associated with increased inflammation and impaired mitochondrial function, meaning the body becomes less efficient at producing energy. These changes can contribute to insulin resistance and push the body toward a pre-diabetic state.
One of the most striking findings is that this form of obesity appears to be independent of diet. Lead researcher Professor Piergiorgio Percipalle said the condition observed in mice occurred regardless of food intake, suggesting a strong genetic influence.
The research indicates that individuals may carry a predisposition to obesity from early life, with symptoms becoming more pronounced over time. It was also found to affect both men and women equally.
Unlike existing weight-loss drugs that primarily suppress appetite, the researchers noted that such treatments often lead to weight regain once stopped, making them temporary solutions rather than long-term fixes.
The team is now working on developing what they describe as “fat tissue reprogramming” therapies—drugs aimed at restoring healthy fat cell function by targeting the underlying genetic mechanisms rather than only controlling appetite.
Clinical applications are still several years away, as further drug development and investment are needed. However, researchers say the long-term goal is to move beyond symptom management and address the biological root causes of obesity.
The findings also carry broader social implications, challenging the long-standing perception of obesity as solely a result of lifestyle or willpower. Instead, the study highlights that genetic and biological factors can play a significant role in how the body stores and processes fat.