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

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

doi:10.1038/s41598-020-59701-0

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

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

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

29 Scopus citations

Abstract

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.

Original language	English
Article number	3035
Journal	Scientific Reports
Volume	10
Issue number	1
DOIs	https://doi.org/10.1038/s41598-020-59701-0
State	Published - 1 Dec 2020
Externally published	Yes

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Publisher Copyright:
© 2020, The Author(s).

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Schulze, F., Wehner, J., Kratschmar, D. V., Makshana, V., Meier, D. T., Häuselmann, S. P., Dalmas, E., Thienel, C., Dror, E., Wiedemann, S. J., Traub, S., Nordmann, T. M., Rachid, L., De Baat, A., Rohm, T. V., Zhao, C., Odermatt, A., Böni-Schnetzler, M., & Donath, M. Y. (2020). Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes. Scientific Reports, 10(1), Article 3035. https://doi.org/10.1038/s41598-020-59701-0

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title = "Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes",

abstract = "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.",

author = "Friederike Schulze and Josua Wehner and Kratschmar, \{Denise V.\} and Valmir Makshana and Meier, \{Daniel T.\} and H{\"a}uselmann, \{St{\'e}phanie P.\} and Elise Dalmas and Constanze Thienel and Erez Dror and Wiedemann, \{Sophia J.\} and Shuyang Traub and Nordmann, \{Thierry M.\} and Leila Rachid and \{De Baat\}, Axel and Rohm, \{Theresa V.\} and Cheng Zhao and Alex Odermatt and Marianne B{\"o}ni-Schnetzler and Donath, \{Marc Y.\}",

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Schulze, F, Wehner, J, Kratschmar, DV, Makshana, V, Meier, DT, Häuselmann, SP, Dalmas, E, Thienel, C, Dror, E, Wiedemann, SJ, Traub, S, Nordmann, TM, Rachid, L, De Baat, A, Rohm, TV, Zhao, C, Odermatt, A, Böni-Schnetzler, M & Donath, MY 2020, 'Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes', Scientific Reports, vol. 10, no. 1, 3035. https://doi.org/10.1038/s41598-020-59701-0

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AU - Schulze, Friederike

AU - Wehner, Josua

AU - Kratschmar, Denise V.

AU - Makshana, Valmir

AU - Meier, Daniel T.

AU - Häuselmann, Stéphanie P.

AU - Dalmas, Elise

AU - Thienel, Constanze

AU - Dror, Erez

AU - Wiedemann, Sophia J.

AU - Traub, Shuyang

AU - Nordmann, Thierry M.

AU - Rachid, Leila

AU - De Baat, Axel

AU - Rohm, Theresa V.

AU - Zhao, Cheng

AU - Odermatt, Alex

AU - Böni-Schnetzler, Marianne

AU - Donath, Marc Y.

PY - 2020/12/1

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N2 - 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.

AB - 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.

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

Abstract

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