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Pancreatic β-cells fine-tune glucose homeostasis through insulin secretion. The endoplasmic reticulum (ER) is critical for insulin production, relying on the unfolded protein response (UPR) to adapt to the body's fluctuating demands. Islets from both type 1 (T1D) and type 2 diabetes (T2D) exhibit inflammation, β-cell dysfunction, and loss. ER stress is present in the inflamed islets of autoimmune diabetes-prone mice and individuals with T1D and T2D. Inflammatory cytokines induce ER stress and disrupt UPR regulation, driving β-cell apoptosis and contributing to diabetes development. Inflammatory cytokines, e.g., IL-1β, impair β-cell function and survival, contributing to diabetes pathogenesis by inducing stress, altering gene expression, driving dedifferentiation, and reducing insulin production. Paradoxically, β-cells exhibit a high density of IL-1R1, and IL-1R1/KO mice display impaired glucose tolerance and reduced insulin secretion. Postprandial IL-1β secreted by macrophages helps maintain blood glucose homeostasis. These observations suggest that circulating low IL-1β concentrations may have physiologically relevant roles; however, their effects on β-cell function and survival remain unclear due to conflicting reports. Preconditioning β-cells with physiological circulating levels of IL-1β (IL-1β^low) induced a resilient state, protecting them from pro-inflammatory cytokine (CYT)-induced cell death while preserving glucose-stimulated insulin secretion through hormesis. IL-1β^low-treated INS-1E cells reduced CYT-induced NO secretion by suppressing NF-κB signaling and decreasing iNOS expression, correlating with reduced β-cell death. IL-1β^low conditioning reduced ER stress and upregulated p-eIF2α in response to CYT, thereby enhancing the expression of ER chaperones and biomarkers linked to improved β-cell identity/functionality. Transcriptomic analysis revealed that IL-1β^low preconditioning mitigated the CYT-induced loss of genes involved in β-cell function/identity, and suppressed the expression of genes linked to NF-κB signaling, cytokine-induced inflammation, and apoptosis. IL-1β^low treatment counteracted the upregulation of stress-related genes triggered by pro-inflammatory stimuli. Enhancing IL-1β^low-induced stress-response hormesis may provide a novel strategy to sustain β-cell function and survival during harmful diabetic inflammation.