IL-1beta promotes the age-associated decline of beta cell function

Summary: Aging is the prime risk factor for the development of type 2 diabetes. We investigated the role of the interleukin-1 (IL-1) system on insulin secretion in aged mice. During aging, expression of the protective IL-1 receptor antagonist decreased in islets, whereas IL-1beta gene expression inc...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Marianne Böni-Schnetzler, Hélène Méreau, Leila Rachid, Sophia J. Wiedemann, Friederike Schulze, Kelly Trimigliozzi, Daniel T. Meier, Marc Y. Donath
Formato: article
Lenguaje:EN
Publicado: Elsevier 2021
Materias:
Q
Acceso en línea:https://doaj.org/article/8c210037d7104ffebcadf66383ce7f6c
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:8c210037d7104ffebcadf66383ce7f6c
record_format dspace
spelling oai:doaj.org-article:8c210037d7104ffebcadf66383ce7f6c2021-11-20T05:08:52ZIL-1beta promotes the age-associated decline of beta cell function2589-004210.1016/j.isci.2021.103250https://doaj.org/article/8c210037d7104ffebcadf66383ce7f6c2021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2589004221012190https://doaj.org/toc/2589-0042Summary: Aging is the prime risk factor for the development of type 2 diabetes. We investigated the role of the interleukin-1 (IL-1) system on insulin secretion in aged mice. During aging, expression of the protective IL-1 receptor antagonist decreased in islets, whereas IL-1beta gene expression increased specifically in the CD45 + islet immune cell fraction. One-year-old mice with a whole-body knockout of IL-1beta had higher insulin secretion in vivo and in isolated islets, along with enhanced proliferation marker Ki67 and elevated size and number of islets. Myeloid cell-specific IL-1beta knockout preserved glucose-stimulated insulin secretion during aging, whereas it declined in control mice. Isolated islets from aged myeloIL-1beta ko mice secreted more insulin along with increased expression of Ins2, Kir6.2, and of the cell-cycle gene E2f1. IL-1beta treatment of isolated islets reduced E2f1, Ins2, and Kir6.2 expression in beta cells. We conclude that IL-1beta contributes the age-associated decline of beta cell function.Marianne Böni-SchnetzlerHélène MéreauLeila RachidSophia J. WiedemannFriederike SchulzeKelly TrimigliozziDaniel T. MeierMarc Y. DonathElsevierarticleCell biologyCellular physiologyPhysiologyScienceQENiScience, Vol 24, Iss 11, Pp 103250- (2021)
institution DOAJ
collection DOAJ
language EN
topic Cell biology
Cellular physiology
Physiology
Science
Q
spellingShingle Cell biology
Cellular physiology
Physiology
Science
Q
Marianne Böni-Schnetzler
Hélène Méreau
Leila Rachid
Sophia J. Wiedemann
Friederike Schulze
Kelly Trimigliozzi
Daniel T. Meier
Marc Y. Donath
IL-1beta promotes the age-associated decline of beta cell function
description Summary: Aging is the prime risk factor for the development of type 2 diabetes. We investigated the role of the interleukin-1 (IL-1) system on insulin secretion in aged mice. During aging, expression of the protective IL-1 receptor antagonist decreased in islets, whereas IL-1beta gene expression increased specifically in the CD45 + islet immune cell fraction. One-year-old mice with a whole-body knockout of IL-1beta had higher insulin secretion in vivo and in isolated islets, along with enhanced proliferation marker Ki67 and elevated size and number of islets. Myeloid cell-specific IL-1beta knockout preserved glucose-stimulated insulin secretion during aging, whereas it declined in control mice. Isolated islets from aged myeloIL-1beta ko mice secreted more insulin along with increased expression of Ins2, Kir6.2, and of the cell-cycle gene E2f1. IL-1beta treatment of isolated islets reduced E2f1, Ins2, and Kir6.2 expression in beta cells. We conclude that IL-1beta contributes the age-associated decline of beta cell function.
format article
author Marianne Böni-Schnetzler
Hélène Méreau
Leila Rachid
Sophia J. Wiedemann
Friederike Schulze
Kelly Trimigliozzi
Daniel T. Meier
Marc Y. Donath
author_facet Marianne Böni-Schnetzler
Hélène Méreau
Leila Rachid
Sophia J. Wiedemann
Friederike Schulze
Kelly Trimigliozzi
Daniel T. Meier
Marc Y. Donath
author_sort Marianne Böni-Schnetzler
title IL-1beta promotes the age-associated decline of beta cell function
title_short IL-1beta promotes the age-associated decline of beta cell function
title_full IL-1beta promotes the age-associated decline of beta cell function
title_fullStr IL-1beta promotes the age-associated decline of beta cell function
title_full_unstemmed IL-1beta promotes the age-associated decline of beta cell function
title_sort il-1beta promotes the age-associated decline of beta cell function
publisher Elsevier
publishDate 2021
url https://doaj.org/article/8c210037d7104ffebcadf66383ce7f6c
work_keys_str_mv AT mariannebonischnetzler il1betapromotestheageassociateddeclineofbetacellfunction
AT helenemereau il1betapromotestheageassociateddeclineofbetacellfunction
AT leilarachid il1betapromotestheageassociateddeclineofbetacellfunction
AT sophiajwiedemann il1betapromotestheageassociateddeclineofbetacellfunction
AT friederikeschulze il1betapromotestheageassociateddeclineofbetacellfunction
AT kellytrimigliozzi il1betapromotestheageassociateddeclineofbetacellfunction
AT danieltmeier il1betapromotestheageassociateddeclineofbetacellfunction
AT marcydonath il1betapromotestheageassociateddeclineofbetacellfunction
_version_ 1718419554206482432