Polymorphisms in insulin regulation and type 2 diabetes: A narrative review of risk and management in Asian populations

The scientific literature extensively discusses the role of single nucleotide polymorphisms (SNPs) in the etiology of type 2 diabetes (T2D). However, the specific mechanisms linking SNPs to T2D remain incompletely understood. Historically, the development of T2D has been attributed to insulin resistance and dysfunction in insulin secretion. The primary aim of this review is to assess the risk of T2D based on its pathophysiology through genetic analysis, with a particular focus on Asian populations, given the ethnic variability in SNPs, and to propose personalized therapeutic strategies. This review identified SNPs involved in insulin regulation, including those related to insulin synthesis and secretion, insulin degradation, peripheral insulin sensitivity, and circadian rhythms. Furthermore, SNPs influencing the response to T2D medications, including biguanides, thiazolidinediones, non-sulfonylurea secretagogues, and sulfonylureas have been identified. Identification of SNPs associated with T2D risk and drug responses suggests that genetic screening could play a key role in both prevention and treatment, offering personalized strategies based on an individual’s genetic profile. Moreover, early identification of SNPs before disease manifestation presents an opportunity for prevention, as epigenetic factors influenced by lifestyle changes may alter disease risk. Further studies are needed to fully understand the mechanisms linking SNPs to T2D and to develop personalized therapies, with a particular focus on Asian populations.