During obesity, the immune system is busy responding to components of bacteria that leak through the intestinal tissue, this results in inflammation, which in turn can drive insulin resistance that can predispose people to diabetes.
“We discovered that during obesity, there are lower levels of a type of B cell in the gut that make an antibody called IgA. IgA is naturally produced by our bodies and is crucial to regulating the bacteria that live in our gut. It acts as a defense mechanism that helps neutralize potentially dangerous bacteria that take advantage of changes to the environment, such as when we consume an imbalanced or fatty diet,” says lead author Helen Luck.
Models deficient in IgA were found to have had worsened blood sugar levels when fed a high fat diet. Gut bacteria taken from those lacking the protective protein transplanted into those with no gut bacteria was found to be able to transfer the disease, demonstrating that IgA can regulate amounts of harmful bacteria in the gut during diet related obesity. Increased levels of IgA were also seen in stool samples from patients after bariatric sugery which supports the importance of IgA and the gut immune system in obese humans.
Findings support a connection between high fat diets, obesity, and lack of IgA in promoting inflammation as well as insulin resistance. This class of antibodies regulates pathogenic bacteria and helps to protect against leaky gut and other obesity related complication, and may be a tool in the fight against diabetes.
“If we can boost these IgA B cells or their products, then we may be able to control the type of bacteria in the gut,” says Dr. Dan Winer of St. Michael’s Hospital. “Especially the ones that are more likely to be linked to inflammation and ultimately insulin resistance. Going forward, this work could form the basis for new gut immune biomarkers or therapies for obesity and its complications, like insulin resistance and type 2 diabetes.”
