According to a recent report by the World Obesity Federation, over four billion individuals will be classified as overweight or obese by 2035.
The study highlighted a growing trend in developing countries across Asia and Africa, where rates of obesity are increasing at a faster pace than in other regions.
Alarmingly, this trend also extends to children, emphasizing the need for urgent action to address this public health crisis.
The global community is confronting an escalating issue of obesity and overweight, with the prevalence continuing to surge.
This situation poses an imminent threat. Unless addressed promptly, countless individuals, including children, face the risk of shorter lives marked by deteriorating health conditions.
Therefore it is really important to understand “what goes wrong in obesity.”
A recent study published in the journal Science Signaling, led by researchers from Maynooth University, has shed light on the role of the metabolic regulator MYC in obesity.
The research focused on MAIT cells, a specific type of immune cells, and revealed that MYC is vital for their growth, proliferation, metabolism, and overall function.
These findings have significant implications for understanding MAIT cells and their involvement in metabolic disorders such as obesity.
Under the guidance of Dr. Andrew Hogan from the Kathleen Lonsdale Institute for Human Health Research, the research team explored the search for a crucial metabolic regulator within MAIT cells.
Their investigations unveiled the essential role of MYC in enabling MAIT cells to acquire and utilize nutrients necessary for their proper functioning.
Interestingly, the study also demonstrated that MYC is defective in individuals with obesity. Previous research by the team has already indicated the impaired functionality of MAIT cells in obesity.
In a previous work last year, the team highlighted the direct contribution of malfunctioning MAIT cells to insulin resistance by disrupting insulin signaling in children affected by obesity.
“In previous papers, we have outlined how the engine of the MAIT cell was defective but we didn’t know why,” comments Dr. Andrew Hogan.
In this new study, they “investigated MAIT cells for a master metabolic regulator and found a protein called MYC is essential for MAIT cell growth, proliferation, metabolism and function.”
They discovered “that MYC helps MAIT cells take in nutrients, which allows them to function.”
“Finally, we found that MYC is defective in people with obesity, providing a mechanism to explain why MAIT cells are defective in obesity.”
This study “shows that MAIT cells are heavily implicated in the development of metabolic disease. Therefore it is of critical importance that we understand how they work and what goes wrong in obesity.”
Dr. Hogan further explained that having identified MYC as a major regulator of MAIT cells and establishing its dysfunction as a primary cause of their defects, the researchers are currently investigating the possibility of targeting MYC to restore normal MAIT cell functions.
This line of inquiry aims to determine if such interventions could be protective against obesity-related complications.
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