Medical

Study finds key gut immune molecule links obesity, the microbiome, and metabolic disorders

New research suggests a high-fat diet lowers the concentration of an important intestinal immune cell that regulates the microbial population in our gut, and it is through this mechanism that obesity can lead to inflammation and diabetes
New research suggests a high-fat diet lowers the concentration of an important intestinal immune cell that regulates the microbial population in our gut, and it is through this mechanism that obesity can lead to inflammation and diabetes
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New research suggests a high-fat diet lowers the concentration of an important intestinal immune cell that regulates the microbial population in our gut, and it is through this mechanism that obesity can lead to inflammation and diabetes
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New research suggests a high-fat diet lowers the concentration of an important intestinal immune cell that regulates the microbial population in our gut, and it is through this mechanism that obesity can lead to inflammation and diabetes

New research led by a team of scientists in Canada has demonstrated how a high-fat diet can disrupt levels of an intestinal immune cell known to help regulate microbial populations in the gut. The study describes how low levels of this molecule result in increased growth of harmful gut bacteria, leading to inflammation and insulin resistance.

Immunoglobulin A (IgA) is a major immune molecule produced by mucosal secretions in the gut. This new study started off with the hypothesis that IgA could be the crucial mechanistic link connecting the gut microbiome with both inflammation and blood sugar levels related to type 2 diabetes.

"IgA is naturally produced by our bodies and is crucial to regulating the bacteria that live in our gut," explains Helen Luck, lead author on the new study. "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."

Using a series of different mouse models the new research demonstrated high-fat diets directly resulted in a drop in IgA levels. The low IgA levels resulted in worsening blood sugar levels, and a higher propensity for leaky gut syndrome.

To test whether these metabolic changes were mediated by gut bacteria, the researchers transplanted the microbiome of obese IgA-deficient animals into germ-free mice with no pre-existing gut microbial population. This indeed did seem to transfer the metabolic phenotype across to the germ-free mice, suggesting the gut microbiome alterations do cause insulin resistance and inflammation.

Looking at human populations the research found fecal IgA levels rising in obese patients following bariatric surgery. This suggests the results should track consistently from animals to humans, particularly in regards to this relationship between diet, IgA levels, and the gut immune system.

While prior research has uncovered compelling interactions between our gut microbiome and our immune system, this is the first study to suggest intestinal homeostasis is regulated by IgA levels. What this means is that combatting diabetes and obesity may involve looking at ways to boost IgA levels.

"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. Especially the ones that are more likely to be linked to inflammation and ultimately insulin resistance," says Daniel Winer, corresponding author on the new research.

The next step for the research is to investigate this mechanism more closely in human subjects to better understand how interconnected IgA deficiency is with obesity, gut microbiome dysbiosis, and metabolic disorders.

The new study was published in the journal Nature Communications.

Source: University Health Network

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