Inhibiting inflammation in “healthy” fat tissue may be key to reversing type 2 diabetes, according to new research.
The study, conducted by researchers from Melbourne’s Walter and Eliza Hall Institute and the RIKEN Institute in Japa, reversed type 2 diabetes in laboratory models by preventing inflammation in certain kinds of fat tissue.
Does inflammation cause type 2 diabetes?
Inflammation is thought to be responsible for the development of insulin resistance, and therefore high blood glucose levels (hyperglycemia), which in turn triggers the development of type 2 diabetes.
Moreover, type 2 diabetes is associated with a number of “lifestyle” factors, such as obesity. The researchers discovered that immune cells known as Tregs prevent the occurrence of inflammation. These Tregs are more prevalent in the fat tissue of people who are of a healthy weight – as obesity develops, the number of Tregs in the fat tissue decreases.
How is inflammation prevented?
The researchers found that certain immune cells – know as regulatory T cells (Tregs) – regulate fat tissue inflammation and control levels of insulin sensitivity. By increasing the presence of Tregs in the immune system, researchers were able to prevent inflammation, and thus impair the development of type 2 diabetes.
In fat tissue, Tregs levels are reduced as obesity develops, thus increasing the likelihood of type 2 diabetes.
The research team found a hormone called IL-33, which can be used to selectively boost the levels of Tregs in fat tissue. If this can be successfully carried out on humans, it may entirely prevent the development of type 2 diabetes.
What do the study’s authors say?
Dr. Ajith Vasanthakumar, one of the study’s authors, said: “When Treg numbers are reduced, inflammatory diseases such as diabetes and rheumatoid arthritis can occur.
“The fat tissue of obese people has lower numbers of Tregs than the fat tissue of people in a healthy weight range. Without Tregs, inflammation-causing cell levels increase, and this rise in inflammation can lead to insulin resistance and high blood glucose levels, a classic hallmark of type 2 diabetes.”
“Treating fat tissues with IL-33 restored normal Treg cell levels, which reduced inflammation and decreased blood glucose levels. Treatments that mimic IL-33 could have the potential to reduce obesity-related inflammation and type 2 diabetes.”
Dr Axel Kallies, another author, said: “We can no longer think of fat tissue simply as energy storage. Fat tissue is increasingly being recognised as a crucial organ that releases hormones and regulates development.
“Keeping our fat tissue healthy is important for our general wellbeing, and our research highlights the important role it plays in preventing disease.”
The research was published in Nature Immunology.

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