Publication: Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation
Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation
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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. (2017). Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nature Immunology, 18(3), 283–292. https://doi.org/10.1038/ni.3659
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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
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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. (2017). Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nature Immunology, 18(3), 283–292. https://doi.org/10.1038/ni.3659