The prevalence of MetS varies, greatly depending on the definition used, gender, age, socioeconomic status, and ethnic background [15]. Thus, the present study aimed to estimate the prevalence of the individual and general components of metabolic syndrome, considering sex-related differences, and assess the impact of age, sex, BMI, education level, and physical activity on the likelihood that participants present the metabolic syndrome. Genetic predisposition can have a great impact on the development of this syndrome, a higher prevalence of MetS has been demonstrated among Hispanic/Latino adults [3].

LEP G2548A and G19A polymorphisms are common genetic variants in people with MetS. These polymorphisms are found in the LEP gene, which encodes a protein that controls appetite and weight regulation. The presence of these polymorphisms may contribute to leptin resistance and, therefore, to obesity and metabolic syndrome [8, 16, 17]. Based on the analysis of genotypic frequencies in the Mexican population, the most common genotype for LEP G2548A was the GA genotype in both study groups, which differs from the frequencies reported in other populations [8]. An interesting observation after adjustment for age, sex, and WC is that the G2548A variant was shown to be associated with MetS in three inheritance models (codominant, recessive, and overdominant) reported in this study in the Mexican population. This is in contradiction with the results of the previous study, in which a relationship between this LEP polymorphism and the risk of MetS was determined [8, 16]. Nevertheless, it is consistent with reports from other populations such as Taiwan and Brazil [18, 19]. The − 2548AA homozygous genotype of LEP carriers had an increased risk for the development of dyslipidemia and − 2548GA shows a protective effect on DM, the biological causes of this are unknown, however, it is known that overdominant models occur when individuals heterozygous for a locus show a higher biological efficacy than individuals homozygous for that same locus, where the most severe manifestation for the disease or health status is when a double dose is received, either normal homozygous or mutated homozygous.

On the other hand, the GA genotype of the LEP G19A polymorphism was also frequently observed in both study groups which agrees with the report in the North Indian Punjabi population [20] and differs from the previous report we found in the literature performed in Egyptian population. In this report conducted in 2020, they describe that this polymorphism is highly associated with obesity and theorize that although it is located in a non-coding region, the association is attributed to its critical position in the 5’UTR regulatory region [20].

Because ADIPOQ regulates metabolism and lipid levels, the potential associations between ADIPOQ SNPs and MetS were also investigated. The ADIPOQ gene provides instructions for making a protein called adiponectin, which regulates glucose levels and fatty acid breakdown in the body. T45G and G276T have been associated with various health outcomes, including obesity, insulin resistance, and type 2 diabetes [21]. Concerning the ADIPOQ T45G and G276T variants in our study, the normal genotype had a higher prevalence among patients in both study groups, and no statistically significant evidence was found that the distribution of genotype frequency was different between the two study groups. This is not to the reports in the Asian population published by Kaur et al., where the most common genotype for the G276T variant was the mutated TT [11]. In the case of the T45G variant, no conclusive information was found on the distribution of genotypes in populations. However, some studies report that the mutated T allele was the most frequent concerning the G allele, which supports our results, where the T allele was the most common in our study populations in both groups [22]. In the ADIPOQ polymorphic variants we are reporting, they were not observed to be associated with MetS, despite adjustment for age, sex, and WC. However, when performing the haplotype analysis, we identified a moderate probability of LD, which is why it was interesting to analyze further detail. The combination in the “ADIPOQ T45G/G276T” haplotype could influence the production, secretion, and function of adiponectin, which in turn could have implications for the risk of developing metabolic syndrome by association with its indicators [23]. In our results, despite differences in the CI for the covariates of hypertension, obesity, and low HDL, such a statistical association was not verified. However, reported ADIPOQ haplotypes that include the T45G and G276T variations, associated with indicators of the MetS, such as type 2 diabetes and obesity, also link their findings with risk factors associated with the disease such as FBG, BMI, and lipid parameters, which suggests its crucial role in susceptibility to metabolic disease [24]. Further research is needed to understand the clinical aspects of genetic variants regulating adiponectin levels in other cohorts.

The frequency distributions of these polymorphisms differ between populations and, therefore, the susceptibility of the individual to the diseases related to these variations. These divergent results could be due to interactions of the polymorphisms with environmental factors, as well as with other polymorphisms present in the LEP and/or ADIPOQ genes, the sample size of a population, or the model used in the statistical analysis.