It is estimated that in Spain there are more than five million people with diabetes, which makes us the second country in Europe with the highest prevalence of this pathology.And worst of all, at least 1.5 million of them ignores it, a figure that, according to experts, everything indicates that it will remain up in the coming years, the result of the current lifestyle and the increase inObesity in our country.
So far it is well known that excess kilos, as well as sedentary lifestyle and inappropriate food are three of the most influential factors when decanting the balance of diabetes development.However, now researchers led by the University of Osaka (Japan) have identified a new mechanism causing this pathology that can change the rules of the game.Specifically, scientists suggest that lack of insulin can be communicated to pancreatic cells that produce it and, therefore, also a possible new therapeutic target for diabetes, as confirmed in a study published today in the magazinescientific «iscience».
It is estimated that type 2 diabetes affects more than 400 million people worldwide and, nevertheless, insulin regulation in the body is not yet fully known.Specifically, type 2 diabetes occurs when the pancreas is unable to supply sufficient insulin, the hormone that controls the use and storage of sugar, to meet the physiological demands.The pancreas cells that produce insulin, known as beta cells, usually proliferate to increase their number if the organism's insulin demand is not satisfied.However, it is unknown what factors are released from tissues or insulin receptor cells to indicate its lack of beta cells of the pancreas.
Now, the researchers discovered that a molecule called T-Cadherina could be involved in the feedback of insulin-producing pancreatic cells and in the control of their proliferation.Thus, the T-Cadherina is usually present on the surface of the cells and is better known for being the joint of a molecule called adiponectin, a factor specifically secreted by the cells that store fat.However, the researchers demonstrated that T-Cadherina is also secreted in soluble forms not described above and can act as a humoral factor, that is, a molecule transported through the circulatory system.Not only did they recognize that the T-Cadherina responds to insulin deficiency, but also demonstrated that genetically modified mice to lack T-Cadherina had a deterioration of glucose tolerance when they were fed with a high-fat diet.
"RNA sequencing analysis, used to investigate gene expression levels throughout the genome revealed a lower expression of notch signaling proteins in beta cells of mice that lack T-Cadherina," explain the main author TomonoriOkita and the corresponding author Shunbun Kita.In this sense, «these proteins play a role in the notch signaling route, which is believed to promote the proliferation of beta cells, this suggests that soluble t-channel send signals to the beta cells of the pancreas to increase the production of the production ofInsulin through the Notch road », details the researchers.
«Next, we use artificially synthesized T-Cadherin to treat pancreatic islets of insulated mouses, which are parts of the pancreas that contain beta cells.This treatment promoted notch signaling in the mouse islets, which in turn could induce the proliferation of beta cells, "explains the principal investigator, who advances that" these findings indicate thatT-Cadherina could be applied in the fundamental treatment of diabetes ».
