New research suggests that certain immune system cells have a significant effect on weight control, potentially influencing the development of type 2 diabetes.
The study, published in Nature, builds on the knowledge that immune cells can help to reduce the risk of obesity in mice, suggesting that the same is true of humans.
The researchers discovered that ILC2 (type 2 innate lymphoid cells) were not as frequent in the belly fat of obese adults as they were for thinner people. The experiments conducted on mice indicate that ILC2s trigger the development of “beige” fat cells, which increase the rate at which the body burns calories.
According to the study, ILC2 cells don’t work properly in the belly fat of obese people. Why this happens is currently unknown: future research will aim to find out. It is hoped that this research will contribute to the development of new methods of tackling obesity.
The research was conducted at Weill Cornell Medical College. Dr. David Artis, leader of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell, said: “Understanding how the immune system regulates metabolism and the function of adipose tissue will help guide investigations into immune-based therapies to limit fat accumulation.
“Of course, a lot more work is needed before we get there, but this study provides significant insights into this pathway.”
Obesity increases the risk of a number of other medical conditions, including type 2 diabetes, coronary heart disease, some kinds of cancer, and stroke.

Get our free newsletters

Stay up to date with the latest news, research and breakthroughs.

You May Also Like

Twice daily dairy intakes could reduce type 2 diabetes risk

Eating cheese, yoghurt or eggs twice a day could help lower the…

Conversation about doctors’ appointments occurring virtually rumbles on

More than half of GP appointments are still being delivered remotely in…

Public Health England considers low carb approach for type 2 diabetes

The low carb approach is being considered by the government to be…