IL-1beta promotes the age-associated decline of beta cell function
Related Experiment Video
Updated: Oct 14, 2025

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Marianne Böni-Schnetzler1,2, Hélène Méreau1,2, Leila Rachid1,2
1Endocrinology, Diabetes, and Metabolism, University Hospital of Basel, 4031 Basel, Switzerland.
Abstract:
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.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
Insulin and C-peptide are...
Insulin Secretory Vesicles
Hormones Regulating Blood Glucose
In addition to accelerating glucose uptake and utilization, insulin has...
Psychoneuroimmunology: Diabetes and Cancer
Tissue Renewal without Stem Cells
However, failure of such a system...

