Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.

Détails

ID Serval
serval:BIB_C7DF25C96E75
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.
Périodique
Nature Immunology
Auteur(s)
Dror E., Dalmas E., Meier D.T., Wueest S., Thévenet J., Thienel C., Timper K., Nordmann T.M., Traub S., Schulze F., Item F., Vallois D., Pattou F., Kerr-Conte J., Lavallard V., Berney T., Thorens B., Konrad D., Böni-Schnetzler M., Donath M.Y.
ISSN
1529-2916 (Electronic)
ISSN-L
1529-2908
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
18
Numéro
3
Pages
283-292
Langue
anglais
Résumé
The deleterious effect of chronic activation of the IL-1β system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1β in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1β, in a glucose-dependent manner. Subsequently, IL-1β contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1β signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1β and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1β mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium-glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1β and insulin in the regulation of both metabolism and immunity.

Pubmed
Web of science
Création de la notice
24/01/2017 19:23
Dernière modification de la notice
03/03/2018 21:20
Données d'usage