Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes
Autor: | Friederike, Schulze, Josua, Wehner, Denise V, Kratschmar, Valmir, Makshana, Daniel T, Meier, Stéphanie P, Häuselmann, Elise, Dalmas, Constanze, Thienel, Erez, Dror, Sophia J, Wiedemann, Shuyang, Traub, Thierry M, Nordmann, Leila, Rachid, Axel, De Baat, Theresa V, Rohm, Cheng, Zhao, Alex, Odermatt, Marianne, Böni-Schnetzler, Marc Y, Donath |
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Rok vydání: | 2020 |
Předmět: |
endocrine system diseases
Interleukin-1beta lcsh:R nutritional and metabolic diseases lcsh:Medicine Chronic inflammation Hormones Article female genital diseases and pregnancy complications Mice Inbred C57BL Diabetes Gestational Disease Models Animal Pregnancy Hyperglycemia Animals Female Steroids lcsh:Q lcsh:Science Gestational diabetes |
Zdroj: | Scientific Reports, Vol 10, Iss 1, Pp 1-11 (2020) Scientific Reports |
DOI: | 10.5451/unibas-ep77878 |
Popis: | Gestational diabetes mellitus (GDM) is one of the most common diseases associated with pregnancy, however, the underlying mechanisms remain unclear. Based on the well documented role of inflammation in type 2 diabetes, the aim was to investigate the role of inflammation in GDM. We established a mouse model for GDM on the basis of its two major risk factors, obesity and aging. In these GDM mice, we observed increased Interleukin-1β (IL-1β) expression in the uterus and the placenta along with elevated circulating IL-1β concentrations compared to normoglycemic pregnant mice. Treatment with an anti-IL-1β antibody improved glucose-tolerance of GDM mice without apparent deleterious effects for the fetus. Finally, IL-1β antagonism showed a tendency for reduced plasma corticosterone concentrations, possibly explaining the metabolic improvement. We conclude that IL-1β is a causal driver of impaired glucose tolerance in GDM. |
Databáze: | OpenAIRE |
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