Diabetes type 2 dysbiosis

The study describes how low levels of this molecule result in increased growth of harmful gut bacteria, leading to diabetes type 2 dysbiosis 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.

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.

The topics include the discussion of the applications in relation to metabonomics and gut microbiota in nutritional research, in health and disease and a review of future therapeutical, nutraceutical and clinical applications.

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 diabetes type 2 dysbiosis relationship between diet, IgA levels, and the gut immune system. While prior research has uncovered compelling interactions between our gut microbiome and our immune systemthis is the first study to suggest intestinal homeostasis is regulated by IgA levels. What this means is diabetes type 2 dysbiosis combatting diabetes and obesity may involve looking at ways to boost IgA levels.

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.