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Introduction {#Sec1} ============ Type 2 diabetes (T2D) is one of the major life-threatening diseases globally, accounting for 4.2 million deaths worldwide in 2019 as assessed by International Diabetes Federation (IDF) consortium^[@CR1],[@CR2]^. According to the IDF report, among 20 countries belongs to the Middle East and North Africa (MENA) region, Iran is ranked third with the highest number of adults (5.4 million) who suffered from diabetes. The prevalence of diabetes in Iran\'s adult population was 11.4% in 2014, estimating 9.2 million Iranian individuals will have diabetes by the year 2030^[@CR3]^. Type 2 diabetes is a common multifactorial metabolic disease, resulting from both genetic and non-genetic (environmental) factors. The heritability of T2D ranges from 20 to 80%, suggesting the considerable role of genetic factors in the development of T2D; the heritable component of the disease is polygenic where many genes and their variants contribute to an enhanced risk of T2D development^[@CR4]^. The advent of high-throughput genotyping technologies has created a significant breakthrough in understanding the underlying genetic components of complex diseases, including T2D. A large number of common and low-frequency T2D susceptibility variants have been characterized by the genome-wide association studies (GWAS) and the whole-genome sequencing^[@CR5]--[@CR9]^. Most of these variants are located near genes that were previously known to be involved in diabetes pathogenesis, such as *TCF7L2, CDKAL1, CDKN1C,* and *IGF2BP2*^[@CR10]^. Among them, *TCF7L2* is responsible for the largest proportion of the T2D-associated variance in the various ethnic groups^[@CR11]^. *TCF7L2* encodes a transcription factor played a central role in the Wnt signaling pathway to regulate glucose homeostasis^[@CR12]^. Since not all individuals are equally affected by type 2 diabetes through the unhealthy lifestyle and some are more sensitive than others, the corresponding genetic variants can lead to the population disparities in the T2D prevalence^[@CR12],[@CR13]^. According to the examination of 16 SNPs, Corona et al. proposed that genetic susceptibility to type 2 diabetes is lower for East Asia and American populations than Africa and Europe populations^[@CR14]^. Similarly, the population differentiation in the obesity-associated variants and the consequent obesity prevalence was reported^[@CR15]^. Nowadays, the availability of population-scale disease-related genetic variants has enabled the researchers to survey the variant frequencies across different populations and estimate the genetic burden of disease. A recent study demonstrated that the high number of deleterious variants attributed to the cardiovascular diseases in Pakistan population can cause the increased mutation load of this disease in the population^[@CR16]^. Considering the complex diseases influenced by many common genetic variants with the small effect size, the meaningful risk assessment requires inspecting the cumulative effect of multiple variants, acquiring with calculating the polygenetic risk score (PRS). Merino et al. computed the polygenic risk score for a large number of diabetic and non-diabetic participants using 68 risk T2D SNPs and indicated that the corresponding genetic burden and the dietary fat quality are associated with the risk of type 2 diabetes^[@CR17]^. Recognizing and targeting the individuals at the highest genetic risk can increase the cost-effectiveness of lifestyle and other interventions to prevent or delay the T2D incidence^[@CR12],[@CR18]^. The