Small Molecules and Epigenetic Modifiers in Facilitating Pancreatic β-cell Formation: A Comprehensive Insight

Diabetes mellitus, arising due to inadequate insulin release or insulin resistance, can be addressed through β-cell replacement therapy. Given the limited availability of islet cadaveric donors, alternative strategies such as differentiation of stem cells into pancreatic β-cells or direct reprogramming of somatic cells into pancreatic β-cells are emerging as viable options. This chapter elucidates the pivotal role of small molecules and associated signaling pathways in in vivo pancreatic organogenesis, allowing their emulation in vitro to facilitate pancreatic development. Small molecules exhibit distinct advantages, such as cell-permeability and non-immunogenic properties, thereby generating efficient functional β-like cells. Recent investigations highlight alterations in epigenetic marks unique to pancreatic β-cells during cellular reprogramming and diabetes pathogenesis. The study further delineates the distinctive histone modifications and DNA methylation within pancreatic β-cells, underscoring their contributions to pancreas development.