We are very happy and grateful to the Novo Nordic Foundation @novonordiskfond that will continue to support our research for the next 5 years! We are delighted to continue our work on the role of somatostatin-producing delta-cells in monogenic diabetes.…
We are very happy and grateful to the Diabetesforbundet forskningsfond @diabetes_no for financing our research! Congratulation, Thomas, for your first grant award! Our research group received funding from Diabetesforbundet forskningsfond the for 2 projects: The effect of human level chemical…
We are very happy and grateful to learn that the Norwegian Research Council @forskningsradet will continue to support our research for the next 5 years! Many plans and experiments are now possible and we are delighted to continue our work…
We are very happy to be partners on a new research project financed under the EEA and Norway Grants scheme promoting research collaboration between Romania and Norway. Our collaborator, Dr. Ana Vacaru from the Institute for Cellular Biology and Pathology…
The Norwegian Research Council announced on 7th of December the new list of awardees. We got new funding from FRIPRO for another independent Young Research Talent project: “Characterizing and modulating the insulin-producing beta-cell fate in monogenic diabetes by using novel…
The second project of the lab is funded by the Research Council of Norway, as a Young Talent Research Project. This 4-year project is aiming at characterizing the cellular and molecular basis of the gradual failure of insulin-producing β-cells in…
Diabetes mellitus is a group of metabolic diseases defined by high blood sugar values caused by the inability of the body to produce and/or use insulin. All forms of diabetes are ultimately characterized by a decrease in the number of functional insulin-producing cells (β-cells), hence a cure for insulin-dependent diabetes types will require their regeneration or replacement. Generally, the most efficient regenerative strategies are the ones involving cell self-renewal capacity. Nevertheless, in mammals, the β-cell proliferative capacity is very low after birth and decreases even further with age. The overall aim of this proposal is to elucidate and reverse the molecular age-switch controlling the gradual impairment of β-cell self-renewal potential by using two murine models of monogenic diabetes.