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Schulze, Friederike; Wehner, Josua; Kratschmar, Denise V.; Makshana, Valmir; Meier, Daniel T.; Häuselmann, Stéphanie P.; Dalmas, Elise; Thienel, Constanze; Dror, Erez; Wiedemann, Sophia J.; Traub, Shuyang; Nordmann, Thierry M.; Rachid, Leila; De Baat, Axel; Rohm, Theresa V.; Zhao, Cheng; Odermatt, Alex; Böni-Schnetzler, Marianne; Donath, Marc Y.

Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes

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  • Medientyp: E-Artikel
  • Titel: Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes
  • Beteiligte: Schulze, Friederike; Wehner, Josua; Kratschmar, Denise V.; Makshana, Valmir; Meier, Daniel T.; Häuselmann, Stéphanie P.; Dalmas, Elise; Thienel, Constanze; Dror, Erez; Wiedemann, Sophia J.; Traub, Shuyang; Nordmann, Thierry M.; Rachid, Leila; De Baat, Axel; Rohm, Theresa V.; Zhao, Cheng; Odermatt, Alex; Böni-Schnetzler, Marianne; Donath, Marc Y.
  • Erschienen: Springer Science and Business Media LLC, 2020
  • Erschienen in: Scientific Reports
  • Sprache: Englisch
  • DOI: 10.1038/s41598-020-59701-0
  • ISSN: 2045-2322
  • Schlagwörter: Multidisciplinary
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>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.</jats:p>
  • Zugangsstatus: Freier Zugang