Background: Emerging evidence suggests that genetic variations in taste receptor genes may influence dietary behaviors, energy homeostasis, and metabolic risk, contributing to type 2 diabetes mellitus (T2DM) pathogenesis. The objective of this study is to evaluate the association between single nucleotide polymorphisms (SNPs) in taste receptor genes and T2DM. Methods: This systematic review followed the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) 2020 guidelines and was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD42022351880). A comprehensive literature search was conducted across PubMed, ScienceDirect, Cochrane Library, and Google Scholar through June 2025. Original studies examining SNPs in taste receptor genes among individuals with T2DM were included. Quality assessment was performed independently by using the Newcastle-Ottawa scale. Results: Sixteen studies involving diverse populations met the inclusion criteria. Significant associations with T2DM were observed for SNPs in type 2 taste receptor gene family R member 3 (TAS2R3; rs11763979), TAS2R4 (rs2233998), TAS2R7, TAS2R9, TAS2R38, TAS2R50, cluster determinant 36 (CD36; rs1761667, rs3211956, rs7755), carbonic anhydrase VI gene (CA6; rs2274327), transient receptor potential vanilloid-1 (TRPV1; rs161364, rs8065080), transient receptor potential cation channel subfamily M gene member 5 (TRPM5; rs4929982), and TRPM8 (rs12472151). These polymorphisms may alter taste perception and gut hormone responses e.g., glucagon-like peptide 1 (GLP-1), affecting dietary intake, satiety, insulin secretion, and glucose regulation. Discussion: The findings suggest that genetic variations in taste receptor genes may contribute to T2DM through behavioral and metabolic mechanisms. Incorporating gustatory phenotyping with genotypic profiling could enable personalized dietary strategies and inform novel therapeutic approaches targeting taste-mediated gut signaling. Further large-scale, multi-ethnic, and mechanistic studies are warranted to confirm these associations and elucidate their clinical implications.
Shivam et al. (Thu,) studied this question.