The pancreatic islets of Langerhans are highly integrated micro-organs composed of distinct endocrine cell types that interact closely to maintain glucose homeostasis. Among these, insulin-secreting β-cells and glucagon-secreting α-cells play dominant roles. Their communication is a multifaceted process involving direct cell-cell contacts, gap junction-mediated electrical coupling, and the exchange of paracrine signals. Recent research has begun to reveal that intercellular signaling within the islet extends beyond the classical view of antagonistic hormone secretion. It encompasses modulatory factors, gap junction interactions, and even hormone-driven plasticity and reprogramming of cell identity. This intercellular crosstalk is especially critical for preserving glucose homeostasis during the progression of diabetes. Our findings show that α-cells actively contribute to islet function not only through glucagon secretion but also by producing the incretin hormone GLP-1, which promotes β-cell survival, proliferation, and insulin secretory capacity-particularly under conditions of compromised insulin output, as seen in diabetes. Additionally, the plasticity of α-cells may underline compensatory responses during β-cell dysfunction. In this lecture, I will present emerging evidence for a revised model of α- to β-cell communication in the diabetic islet, highlighting how dynamic intercellular signaling mechanisms adapt to support islet function when insulin secretion becomes insufficient.

IPHYS contact person: Lydie Plecitá-Hlavatá, lydie.plecita@fgu.cas.cz