The study, by a group of researchers from University of Oxfordhas focused on how high blood sugar leads to insulin resistance or intolerance and has concluded that the intermediate step between unhealthy factors and damage to the insulin-producing beta cells of the pancreas is not yet fully understood.
As explained Elizabeth HaythorneThe main author of the study had already confirmed in earlier work that the chronic hyperglycemia it is the one that causes the damage in the beta cells; However, it remained to be clarified how this process occurs and how it would be possible to stop this damage at one of its stages.
Through a series of animal and laboratory-grown cell studies, researchers have discovered that it is not excess glucose per se that is responsible for the poor functioning of insulin-producing beta cells; but the metabolitesthe products produced by the sugar metabolism.
It is currently unknown which specific glucose metabolites initiate the process; However, inhibiting metabolism has managed to sustain insulin production even in high blood sugar environments.
Although it sounds counterintuitive, researchers have found that blocking glucose metabolism by inhibiting an enzyme called glucokinase increases insulin secretion.
In theory, normal glucose metabolism stimulates insulin secretion. Previously it would have been thought that increasing it might improve insulin production in type 2 diabetes, but now these results suggest that insulin activators glucoquinase could lead to an adverse effect.
Actually, the best treatment would be the opposite: suppression. For now, the researchers have cautioned that their results are preliminary and will not change the therapeutic approach until the results are confirmed in humans.
However, if this finding is confirmed by future studies, it could be groundbreaking and completely rethink both the treatment and management of type 2 diabetes. in addition to the fact that beta cell dysfunction could be delayed and even prevented with treatments pointing in the opposite direction to current therapies.