Joint investigation of Gothenburg and Girona universities accounts for the mechanism of action of the most effective therapy against type 2 diabetes, through the "makeup" of intestinal bacteria.The document in this regard was published by Nature Medicine.
Metformin is prescribed to reduce the amount of glucose produced by the liver to help people with type 2 diabetes control their blood sugar.But the mechanism is more complex than this.The slow -release metformin seems to be so effective despite the fact that only small amounts of it reach the liver, even in people with genetic variants that prevent it from reaching the liver.
This raised the suspicions that the billions of intestinal bacteria would be the agents of the drug action.
The team recruited 40 volunteers with type 2 diabetes, whom it was randomly assigned to take metformin or a placebo for four months.All of them were placed in a low calorie diet.
During the study period, the composition of intestinal bacteria changed much more dramatically in those who take metformin.The drug seemed to stimulate the growth of bacteria strains called akkermansia and bifidobacterium.
The researchers then took stool samples of three people before and after a metformin course and fed them to mice that were in a high fat diet, to imitate human type 2 diabetes in a technique known as fecal transplant.
The feces of the individuals with metformin seemed to improve glucose tolerance in mice that received samples of two of the three donors.But the feces taken from people before their treatment had no effect on any of the mice.
Although the team was able to register the high levels of the mentioned bacterial strains, the researchers still do not know how they could be interacting with the drug and their therapeutic action.However, it is the primee step for the establishment of diets and therapies that promote the growth of the referred akkermansia and bifidobacterium in order to improve the quality of life of those who suffer from this type of diabetes.
A pill taken daily, developed last March, reverses the symptoms of diabetes in mice, opening the possibility of developing a drug for humans, which maintains blood sugar levels within safe limits by affecting receptors of receptorsinsulin in the liver.
