Chakravarthy et al. dissect the mechanisms maintaining α cell identity and reveal that simultaneous inactivation of the DNA methyltransferase Dnmt1 and the transcription factor Arx in adult mice drives the conversion of α- to β-like cells. In human T1D islets, glucagon+ cells lose DNMT1 and ARX expression and express β cell markers.
Here, we discuss the latest findings on pancreas and islet cell plasticity upon physiological, pathological and experimental conditions of stress. Understanding the mechanisms involved in cell reprogramming will allow the development of new strategies for the treatment of diabetes, by exploiting the intrinsic regeneration capacity of the pancreas.
The prevalence of diabetes will rise from 2.8% of the total world population in 2000 to 4.4% in 2030. The two prevailing forms of diabetes, named Type 1 and Type 2 (T1D and T2D), are chronic and often lead to…
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…
Yesterday it was announced the new members affiliated with NCMM and the Nordic EMBL Partnership in Molecular Medicine, following an open call announced in the spring and with deadline in September, and to our greatest pride, Simona is one of…
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.