Type 2 diabetes
Diabetes is a chronic disease related to dysfunction in the production or use of insulin, a hormone that regulates blood sugar. The gastrointestinal microbiota has been identified as one of the environmental factors that may be to blame.
About this article
In 2015, 415 million people had diabetes. According to WHO forecasts, it will be 642 million in 2040. Ninety percent of cases are type 2 diabetes.
Insulin resistance, the primary cause of type 2 diabetes
The primary cause of type 2 diabetes is cells in the body losing their sensitivity to insulin. This resistance to insulin makes the hormone ineffective and leads the pancreas to produce more, to the point of exhaustion. As a result, sugar accumulates in the blood, leading to hyperglycemia and serious long-term complications: myocardial infarction, stroke, arteritis in the lower limbs, kidney failure, and blindness.
Involvement of the intestinal microbiota?
Although there is a genetic component to type 2 diabetes, lifestyle is the biggest risk factor for the disease--especially sedentism and a diet including too much fat and sugar. Certain fats and sugars set off an inflammatory response associated with metabolic disorders, which in turn increase the level of inflammation. It starts a vicious cycle, in which the gastrointestinal microbiota contributes because it is unbalanced. Researchers have shown that the gastrointestinal microbiota is disrupted in diabetics, and that this dysbiosis contributes to the disease.
Above all, diabetes is treated by making lifestyle improvements: weight loss if necessary, regular physical activity, and a balanced diet. It is often necessary to add medication.
The role of certain intestinal bacteria and/or probiotics in diabetes has yet to be confirmed, but their beneficial effects (particularly on appetite and blood sugar) have opened a path for the development of new therapeutic targets for this disease, which affects millions of people.
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Serino M, Luche E, Gres S, et al. Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota. Gut, BMJ Publishing Group, 2012 ; 61 : 543-53. https://hal.archives-ouvertes.fr/inserm-00726182/document