The mechanisms that restrict regeneration and maintain cell identity following injury are poorly characterized in higher vertebrates. Following β-cell loss, 1-2% of the glucagon-producing α-cells spontaneously engage in insulin production in mice. Here we explore the mechanisms inhibiting α-cell plasticity.…
We have the pleasure of hosting Dr. Natalia Soshnikova from the Institute of Molecular Biology (IMB), Mainz, Germany. She will talk about the molecular mechanisms of intestinal stem cell specification during development on 18th of January 2018 at BUS1 Pankreas…
Current published protocols for targeted differentiation of human stem cells toward pancreatic β-cells fail to deliver sufficiently mature cells with functional properties comparable to human islet β-cells. We aimed to assess whether Wnt-modulation could promote the final protocol stages of…
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…
If you want to read about our research featured in an article published on the News of University of Bergen, please click on the following link: Studying single-gene disorders to cure diabetes
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.
MODY (maturity-onset diabetes of the young) is caused by pancreatic beta cell dysfunction due to a single gene mutation affecting both the prenatal and postnatal pancreas development. Importantly, more than 90 % of MODY mutation carriers will develop diabetes during…