For the first time, UAB researchers have cured mice with diabetes type 1
A team of researchers from the Universitat Autònoma de Barcelona (UAB) has cured mice with diabetes type 1 for the first time. In the experiment, the diabetic mice completely recovered from the disease after having suffered excesses of glucose in their blood. Although the mice used were transgenic, the researchers are sure that there will soon be a genic therapy based on this discovery that will cure non-transgenic mice with diabetes type 1, and which, within a few years, will also be able to cure people. The study was published in last edition of Journal of Clinical Investigation.
A research team led by Fatima Bosch, professor in the Department of Biochemistry and Molecular Biology at the UAB, has studied the effects of protein IGF-I on mice with diabetes type 1, i.e. the type of diabetes produced by a decrease in the number of beta cells in the pancreas, the ones which produce insulin. In order to study this effect, the researchers used mice that were genetically modified so that the beta cells in their pancreases would produce protein IGF-I, and have compared the development of diabetes type 1 in this type of mice to the evolution of the disease in control mice (without genetic modifications).
The results of the experiments clearly show that in the transgenic mice with the gene that codifies for protein IGF-I activated in beta cells, the induction of experimental diabetes leads to the replication of these cells, their programmed cellular death is counteracted (apoptosis) and the resident mother cells in the conducts of the pancreas are induced to develop insulin-producing beta cells. All these effects lead to the mice completely recovering from the disease, re-establishing absolutely normal levels of glucose in their blood.
The team of UAB scientists chose to experiment with this protein because it has provided excellent results in vitro – it causes the replication of beta cells and counteracts apoptosis – and moreover, mice in which there is destruction of the gene that codifies the IGF-I receptor have very small pancreatic islets (the conglomerates of the beta cells in the pancreas).
This is the first time in which it has been demonstrated that a curative therapy for diabetes is possible, and could imply important advantages over other therapies that are currently being investigated, such as the transplant of islets or beta cells cultivated in vitro. Moreover, in the therapy developed by Doctor Fatima Bosch’s team, the effect of IGF-I does not occur until the animal suffers the destruction of its beta cells. Therefore, non-diabetic transgenic animals are perfectly normal, without any alterations or secondary effects.
The researchers are sure that the next stage of the research programme, the curing of normal (i.e. non-transgenic) mice with diabetes 1 by mean of genic therapy, will probably take place in the near future. Once the scientists have successfully carried out tests with experimental animals, they will be able to consider applying the technique to humans, although this will not be for some time. In order to cure diabetes type 1, viral vectors (innocuous viruses) carrying the gene that codifies for IGF-I will have to be injected into the pancreas.
The research, published in last edition of Journal of Clinical Investigation, has involved the participation of researchers from the Department of Biochemistry and Molecular Biology at the UAB, specifically the Unit from this department based in the Faculty of Veterinary Science, along with members of the Centre for Animal Biotechnology and Genetic Therapy (CBATEG) at the Biocampus research complex of the Universitat Autònoma de Barcelona. The research was financed by the Fondo de Investigación Sanitaria (Health Research Fund), the Plan Nacional de I+D (National R&D Plan) of the Spanish Ministry for Education and Culture, the TV3 Marató Foundation, the Generalitat de Catalunya’s General Research Management and the European Community Training and Mobility Program.
Octavi López Coronado | alphagalileo
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