An important study shows that the fermentation activity of intestinal bacteria generates certain fatty acids that block the development of type 1 diabetes.
Type 1 diabetes is an autoimmune disease caused by the specific destruction of pancreatic cells responsible for insulin production. There is a strong genetic predisposition to this immune dysregulation, but more and more observations indicate that other factors associated with lifestyle (diet, excessive hygiene, overuse of antibiotics) could also contribute to the development of this disease. The increase in the incidence of Type 1 diabetes observed in recent decades could therefore be a consequence of certain changes in lifestyle that have occurred during this period, which suggests that it is possible to prevent this disease. by certain lifestyle changes.
Gut imbalance promotes type 1 diabetes
It is now well established that the intestinal microbiota, that is to say the vast bacterial community that lives in the intestine, and more particularly in the colon, plays a leading role in the proper functioning of the immune system.
Studies show that changes in the composition of the microbiota are associated with immune disorders such as inflammatory bowel disease, multiple sclerosis, allergies and asthma, suggesting that this microbiota may also play a role in autoimmunity responsible for type 1 diabetes. This influence seems to be due to the ability of these bacteria to metabolize dietary fiber to generate short-chain fatty acids, such as acetate and butyrate, which are formed in very large quantities in the colon. These fatty acids increase the activity of regulatory T lymphocytes essential for maintaining immune tolerance, stabilize the intestinal barrier to limit the infiltration of bacteria into the blood and also possess anti-inflammatory activity.
This therefore suggests that an increase in the fermentation activity of the microbiota could stabilize immune function and prevent the development of an autoimmune response leading to the destruction of pancreatic cells involved in insulin production.
Fiber and fatty acids protect against type 1 diabetes
This hypothesis is reinforced by the results of a study recently published in the prestigious Nature Immunology. To examine the impact of an increase in short-chain fatty acids on the risk of diabetes, a team of Australian scientists came up with the idea of feeding animal models with sources of starches biochemically modified with acetate. or butyrate. These starches resist digestion by the stomach, but are subsequently fermented in the colon by intestinal bacteria and release large amounts of these fatty acids. It is therefore an interesting model for reproducing the formation of acetate and butyrate that occurs during the fermentation of dietary fibers by the intestinal microbiota.
The researchers first observed that each of these starches (enriched with acetate or butyrate) provided marked protection against the development of type 1 diabetes. On the one hand, the diet enriched with acetate causes a marked decrease in white blood cells (T cells) which possess autoimmune activity, while elevated butyrate production improves the function of regulatory T cells. When these two types of starches are administered simultaneously, these combined actions ensure that the destruction of insulin-producing cells is completely blocked and therefore the development of diabetes is halted.
These observations therefore suggest that the metabolites generated by the fermentation activity of intestinal bacteria, the short-chain fatty acids in particular, exert extremely positive effects on the proper functioning of the immune system. Since dietary fibers are the preferred “food” of these bacteria, a plant-rich diet including fruits, vegetables, legumes and whole grain cereals is the best way to optimize the metabolic function of this microbiota and thus reduce the risk of autoimmune diseases, including type 1 diabetes.
Mariño E et al. Gut microbial metabolites limit the frequency of autoimmune T cells and protect against type 1 diabetes. Nat. Immunol; 18: 552-562.