New research – using mouse models and fecal samples collected from humans – looks into the mechanisms that promote insulin resistance through the gut environment. The kind of diet a person eats may be important, the researchers suggest.
Insulin resistance occurs when the body stops reacting normally to insulin, a hormone that helps the body process sugar.
Developing insulin resistance can lead to type 2 diabetes, a metabolic condition that affects millions of people worldwide.
Obesity is an important risk factor for insulin resistance and diabetes. But how and why does obesity drive metabolic changes?
Researchers at the University of Toronto in Canada believe the answer may lie in mechanisms that consume high-fat diets.
“During high-fat diet feeding and obesity, there is a significant change in the microbial population of the gut, known as dysbiosis, which interacts with the intestinal immune system,” the researchers published in their Nature Communications The new study paper is explained.
The team decided to try and figure out how high-fat diets could alter gut immunity and, thus, balance bacteria, leading to insulin resistance.
The researchers wrote in their paper, “The link between the gut microbiota and the intestinal immune system is the immune derived molecule immunoglobulin A (IgA).” They say that this molecule is an antibody produced by B cells, which are a type of immune cells.
Investigators thought that IgA may be the missing link, suggesting how a poor diet leads to insulin resistance by altering intestinal immunity.
A sensitive mechanism affected by diet
In the first part of their study, investigators used mouse models with obesity, some of which lacked IgA. Researchers found that when IgA-deficient mice ate a high-fat diet, their insulin resistance deteriorated.
When researchers collected intestinal bacteria from IgA deficient mice and transplanted them into rodents without gut bacteria, these mice also developed insulin resistance.
This experiment, researchers suggest, will help keep IgA gut bacteria in check, at normal levels. Not only that, but it will also help prevent harmful bacteria from “leaking” through the intestines.
Mice without IgA had increased gut permeability, meaning that harmful bacteria could “leak” from the gut to the rest of the body.
Following these experiments in preclinical models, the researchers proceeded to see if the same mechanism applied to humans. They were able to obtain stool samples from individuals who had bariatric surgery – a form of surgery for weight loss.
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Researchers analyzed the content of IgA in fecal samples collected both before and after individuals underwent bariatric surgery.