A study led by the VIB Institute in Flanders, Belgium, has just identified a common genetic basis for type I diabetes and type II diabetes, which could improve the design of therapies and drugs for this metabolic disease.
A study reveals a common genetic basis for type I diabetes and type 2 diabetes, based on fragility induction in insulin producing cells.Image: London Science Museum.Image: John Goode (CC By 2.0).
Diabetes encompasses different metabolism disorders characterized by the inability to regulate blood glucose levels as a consequence of insulin production defects by beta-pancreatic cells.Type I diabetes, the result of autoimmune destruction of insulin producing cells, shares common clinical features with type 2 diabetes, in which metabolic changes give rise to the body resistant to insulin.However, both entities have been considered as extremes of the disease, in terms of the molecular causes that cause it.
Using a diabetes model in Mouse, the VIB Institute researchers identified a series of genetic components that increase the predisposition to the two main types of diabetes, through a mechanism that induces fragility in beta-panematic cells independentlyimmune system action.These components are genetic variants in the XRCC4 gene and altered expression of the GLIS3 gene.Both genes intervene in molecular routes also identified after the expression analysis in patient samples.
"Thanks to our genetic component, some of us have beta cells that are resistant and strong, while others have beta cells that are fragile and cannot handle stress," says Adrian Liston, labor director."The latter are those that develop diabetes, type 1 or type 2, while those with more resistant beta cells will remain healthy even if they suffer from autoimmunity or metabolic dysfunction of the liver."
In addition, the team demonstrated the ability of the fat -rich diet to replace the genetic component in the acceleration of death and senescence of insulin -producing pancreatic cells, in a mouse strain resistant to insulin.This confirms, once again, that diet is an important factor in the development of diabetes.
The new work identifies the failure or fragility of beta-pancreatic cells as a common mechanism in the two main types of diabetes.In this sense, the team states that in the case of type 1 diabetes, the initial development of the pathology is mediated by an autoimmune process, while the subsequent loss of beta-pancreatic cells derives from stress to which thecells that remain, to produce sufficient insulin levels.
The results of the study have important applications both to know better the biological basis responsible for diabetes and to investigate new treatments for it."This new model in mouse will allow us, for the first time, to test new antidiabetic drugs focused on preserving pancreatic beta cells," says Liston."There are many promising drugs in development in biomedical companies that were waiting to have an animal model."
Reference: Dooley J, et al.Genetic predisposition for beta Cell Frady Underlies Type 1 and Type 2 Diabetes.Nat Genet.2016 Mar 21. Doi: 10.1038/Ng.3531.
Source: New Study May Lead To Improved Treatment of Type 2 Diabetes. Link
