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

First Author  Schulze F Year  2020
Journal  Sci Rep Volume  10
Issue  1 Pages  3035
PubMed ID  32080229 Mgi Jnum  J:293486
Mgi Id  MGI:6407328 Doi  10.1038/s41598-020-59701-0
Citation  Schulze F, et al. (2020) Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes. Sci Rep 10(1):3035
abstractText  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-1beta (IL-1beta) expression in the uterus and the placenta along with elevated circulating IL-1beta concentrations compared to normoglycemic pregnant mice. Treatment with an anti-IL-1beta antibody improved glucose-tolerance of GDM mice without apparent deleterious effects for the fetus. Finally, IL-1beta antagonism showed a tendency for reduced plasma corticosterone concentrations, possibly explaining the metabolic improvement. We conclude that IL-1beta is a causal driver of impaired glucose tolerance in GDM.
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