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New indications of prenatal environmental factors affecting risk of developing type 1 diabetes

A new study by the Immunology of Diabetes Group, led by Marta Vives-Pi at the IGTP-UAB in collaboration with the University Hamburg-Eppendorf, looks into the effect of betamethasone on new-borns and its susceptibility to develop type 1 diabetes, when it is administered before birth. As well as corroborating the previous results and finding new changes in the developing immune system, the results also throw light onto the effect of the drug on the insulin-producing cells themselves.
The research team.

Type 1 diabetes mellitus (T1D) is caused by the destruction of the pancreatic cells that produce insulin (β-cells), which are part of the mechanism that controls the storage and use of sugar in the blood. It is normally diagnosed in childhood or adolescence and the incidence is increasing by 4% per year. Both genetic and environmental factors play a role but the cause of the disease is still difficult to define.

Betamethasone is a widely used drug in pregnant women at risk of preterm delivery to improve the survival of new-borns. Previous studies have shown that it can affect the behaviour of the immune system cells. To assess the effect of betamethasone, the group used a type of mouse that spontaneously develops T1D and that is considered the experimental model for the study of the human disease.

This work, carried out by David Perna-Barrull, under the direction of Marta Vives-Pi in the Immunology of Diabetes Group at the IGTP (Institut d’Investigació Germans Trias i Pujol) in collaboration with researchers from the University Medical Center Hamburg-Eppendorf, has painstakingly looked at the effects of Betamethasone in the developing immune system. The results confirm a protection against T1D after betamethasone administration. Changes included alterations in white blood cells and the failure of some cells that participate in the autoimmune response causing T1D to mature. Moreover, the group described the effect of the drug on the β-cells, by reducing insulin secretion, and altering the expression of genes related to autoimmunity and metabolism. In summary, prenatal betamethasone exposure might alter the immune system and β-cells in developing mice, thus decreasing the risk of developing T1D in mice. Given the increase in the incidence autoimmune disorders in the last years, elucidating the mechanisms of action of prenatal glucocorticoids will help to design prevention strategies.

Dra. Marta Vives-Pi
Institut d’Investigació Germans Trias i Pujol
Universitat Autònoma de Barcelona


Perna-Barrull, David & Rodríguez Fernández, Silvia & Pujol-Autonell, Irma & Gieras, Anna & M. Ampudia-Carrasco, Rosa & Villalba, Adrián & Glau, Laura & Tolosa, Eva & Vives-Pi, Marta. (2019). Prenatal Betamethasone interferes with immune system development and alters target cells in autoimmune diabetes. Scientific Reports. 9. DOI: 10.1038/s41598-018-37878-9.

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