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. |