Molecular, genetic, and pharmacological advances in type 2 diabetes (2015-2025)

Type 2 diabetes (T2D) is a multifactorial metabolic disorder driven by the interplay of insulin resistance, β-cell dysfunction, and complex genetic and epigenetic factors. Over the past decade (2015-2025), advances in molecular biology, genomics, and pharmacology have reshaped our understanding of its pathogenesis and treatment. Large-scale GWAS and functional genomics have clarified genetic risk loci and epigenetic mechanisms, while novel biomarkers, including circulating microRNAs and metabolomic signatures, offer potential for early detection and risk stratification. Therapeutically, incretin-based drugs, especially GLP-1 receptor agonists and dual agonists, as well as SGLT2 inhibitors, have transformed outcomes by targeting both glycemic control and cardiovascular-renal protection. These insights have also informed prevention strategies, emphasizing weight reduction, microbiome modulation, and precision interventions based on genetic risk. Yet major gaps remain, including functional annotation of risk loci, understanding of β-cell dedifferentiation and recovery, and equitable implementation across diverse populations. This review synthesizes molecular, genetic, and pharmacological progress from 2015 to 2025, highlights clinical translation, and identifies priorities for the next decade of research.