Association of Vaspin rs2236242 with Metabolic Syndrome: A Meta-Analysis of Case

Abstract

Background/purpose of the study:

Metabolic syndrome (MetS) is a multifactorial condition characterized by central obesity, insulin resistance, dyslipidemia, and hypertension, all of which increase the risk of cardiovascular disease and type 2 diabetes mellitus. Genetic variants affecting adipokine signaling, such as polymorphisms in the vaspin gene (SERPINA12), have gained attention due to their potential role in modulating metabolic traits. Among these, the single nucleotide polymorphism rs2236242 (T>A) has shown conflicting associations with MetS across populations. This study presents the first comprehensive meta-analysis investigating the association between rs2236242 polymorphism and MetS susceptibility.

Methods:

We searched PubMed, Google Scholar, Scopus, and Web of Science for relevant articles published up to 12 December 2025. Data were extracted, and summary estimates of the association between vaspin rs2236242 and MetS were assessed. Odds ratios (ORs) and confidence intervals (CIs) were used to measure the effect. Four eligible case-control studies involving 918 participants from Caucasian, African, and Western Asian populations were included.

Results:

Our results demonstrate that the A allele of rs2236242 is significantly associated with a 37% reduced risk of MetS compared to the T allele, with consistent protective effects observed across multiple genetic models (dominant, recessive, homozygous, and heterozygous). These findings align with previous studies suggesting the metabolic benefits of vaspin, including improved insulin sensitivity. Moreover, sensitivity analyses identified the study by Suliga et al. as an outlier, its exclusion reduced heterogeneity to 0% while maintaining the significance of the protective association.

Conclusion:

We performed the first meta-analysis on the association of vaspin rs2236242 with MetS and found that the vaspin rs2236242 A allele confers a significant protective effect against MetS.

Keywords

metabolic syndrome vaspin SERPINA12 rs2236242 single nucleotide polymorphism

Introduction

Metabolic syndrome (MetS) represents a complex metabolic condition characterized by the coexistence of interrelated metabolic abnormalities, including central obesity, insulin resistance, dyslipidemia, and hypertension.¹ The clustering of these abnormalities markedly increases the likelihood of developing cardiovascular disease and type-2 diabetes mellitus (T2DM), thereby imposing a substantial burden on global health systems.² The prevalence of MetS has escalated worldwide alongside rising obesity rates, largely attributable to physical inactivity, energy-dense diets, and rapid urbanization. A recent meta-analysis using the Joint Interim Statement criteria estimated a global prevalence of 31.4%, with rates reaching 34.1% in upper–middle-income countries and 29.5% in the Western Pacific region.³ Given its association with increased all-cause mortality and long-term cardiometabolic complications,⁴ a deeper understanding of the molecular mechanisms underlying MetS is crucial for improving risk stratification, early detection, and the development of personalized therapeutic strategies.

Growing evidence highlights adipose tissue as an active endocrine organ that secretes a range of bioactive mediators known as adipokines, which play pivotal roles in metabolic regulation and inflammatory signaling.⁵ Among these adipokines, vaspin (visceral adipose tissue-derived serpin), encoded by the SERPINA 12 gene located on chromosome 14q32.13, has garnered interest for its potential insulin-sensitizing and anti-inflammatory properties.⁶ Vaspin was first identified in the visceral adipose tissue of Otsuka Long-Evans Tokushima Fatty rats, a well-established animal model of obesity and T2DM, and has since been detected in human subcutaneous adipose tissue.⁷ Experimental studies demonstrate that administration of recombinant vaspin improves glucose tolerance and enhances insulin sensitivity in obese murine models.⁸ In clinical settings, circulating vaspin concentrations have been associated with obesity, insulin resistance, and several individual components of MetS, although reported findings remain inconsistent across populations.⁹

Single nucleotide polymorphisms (SNPs) in SERPINA 12 may contribute to inter-individual differences in vaspin expression and function. Notably, the rs2236242 variant (T>A) was selected for this investigation because it is a missense mutation located in a functional region of the gene, potentially altering protein stability or secretion, thereby directly influencing metabolic traits. This SNP is one of 26 tagged variants that comprehensively encompass the SERPINA 12 locus.¹⁰ Prior studies have yielded mixed results regarding its association with obesity, insulin sensitivity, and plasma vaspin levels.¹¹ Although a recent meta-analysis reported a protective association between rs2236242 and obesity susceptibility,¹² no significant relationship was observed with T2DM risk. Notwithstanding that, several studies have suggested a link between rs2236242 and MetS. Hashemi et al. were the first to report such an association,¹³ with corroborative findings later provided by Alnory et al. and Mehanna et al.¹⁴ Other studies, however, have reported negative findings, highlighting inconsistencies that may stem from differences in ethnicity, study design, sample sizes, or the diagnostic criteria used to define MetS.

To date, no meta-analysis has specifically and systematically evaluated the association between the SERPINA 12 rs2236242 polymorphism and susceptibility to MetS. Addressing the knowledge gap is necessary to clarify the genetic contribution of vaspin to metabolic dysfunction. Therefore, the present study aimed to perform the first meta-analysis of case-control studies to quantitatively assess the relationship between the rs2236242 variant and MetS risk. The findings of this study may enhance current understanding of the genetic architecture of MetS and support the future development of genetic biomarkers for personalized metabolic risk assessment.

Methods

Search strategy

A comprehensive literature search was conducted to identify studies evaluating the association between vaspin rs2236242 and MetS. Electronic databases, including PubMed, Google Scholar, Scopus, and Web of Science, were systematically searched, with the most recent update performed on 12 December 2025. The search strategy followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.¹⁵ The following keyword combinations were used: “(vaspin OR SERPINA12) AND (genetic variation OR polymorphism OR SNP) AND (metabolic syndrome OR obesity OR dyslipidemia OR diabetes OR type 2 diabetes mellitus).” Additionally, reference lists of relevant original articles and review articles were manually screened to ensure comprehensive coverage.

Study eligibility

Studies were included if they met the following criteria: (i) full-text articles available in a readable and interpretable format; (ii) MetS defined as the primary outcome; (iii) evaluation of the association between the rs2236242 polymorphism and MetS; (iv) case–control study design; and (v) sufficient genotype data to calculate odds ratios (ORs) with 95% confidence intervals (CIs). Studies were excluded if they: (i) lacked accessible or comprehensible full text; did not focus primarily on MetS; (iii) investigated SERPINA12 polymorphisms other than rs2236242; (iv) used non-case-control designs; or (v) provided insufficient data for statistical analysis.

Data extraction and quality score assessment

Data extraction was independently performed by two investigators (Wei-Yue Lim and Amira Elina) using standardized extraction forms. Initial screening was conducted based on titles and abstracts, followed by full-text evaluation where eligibility was uncertain. Any discrepancies were resolved through discussion, with consultation from a third reviewer (Shamsul Mohd Zain) when necessary. The methodological quality of the included studies was assessed using the Newcastle–Ottawa Scale, which evaluates study selection, comparability of study groups, and outcome assessment.¹⁶ Scores were given on a scale from 0 to 9, with studies receiving a score of 7 or above, categorized as having high quality. The details of the PRISMA criteria and follow diagram used are provided in Supplementary Tables S1 and Supplementary Fig S1.

Statistical analysis

Meta-analysis was carried out using the Review Manager (RevMan 5.4, The Cochrane Collaboration, Copenhagen, Denmark) of the Cochrane Collaboration. The primary outcome of this study was the pooled estimates for MetS occurrence. Hardy-Weinberg equilibrium of the genotypes from each individual study was determined using a χ²-test, with deviance defined as P < 0.05. The pooled ORs and their corresponding 95% CIs were calculated using the Mantel-Haenszel test, under the assumption of a random-effect model. The forest plot was visually inspected to measure the study heterogeneity and further analyzed by the χ²-test of heterogeneity (a significant test for heterogeneity) and the inconsistency index I2 (the magnitude of heterogeneity). A χ²-test of P < 0.10 and I2 values exceedingly more than 50% were employed to indicate heterogeneity. A fixed-effect model was used when the heterogeneity was little or nonexistent (I2 values < 25%); a random-effect model was used if the heterogeneity was greater (I2 values > 25%) (Higgins et al., 2003).

Publication bias and sensitivity analysis

Potential publication bias was assessed by visual inspection of funnel plot symmetry and quantitatively evaluated using Begg and Mazumdar’s rank correlation test and Egger’s linear regression test, performed in R software (version 4.0.5).^17,18 Sensitivity analyses were conducted by sequentially excluding individual studies to examine their influence on pooled effect estimates. Statistical significance was defined as a two-tailed P value < 0.05.

Results

Study selection and characteristics

The study selection process is illustrated in (Fig. 1). A total of 31 articles were identified through the initial database search, with an additional 16 retrieved from external sources. After applying the predefined search criteria, 47 articles were initially considered. Following the exclusion of five review articles and 29 studies based on title and abstract screening, 13 articles remained for full-text evaluation. Of these, nine were subsequently excluded for reasons detailed in Figure 1 including: investigation of other SERPINA12 polymorphisms (n = 1) and outcome was not MetS (n = 8). This resulted in four eligible studies for meta-analysis on vaspin rs2236242 and its association with MetS.

FIG. 1.

Flow chart showing study selection procedure.

Table 1 summarizes the characteristics of the included studies, which were published between 2012 and 2019 (Table 1). The four studies encompassed sample sizes ranging from 100 to 151, with a combined total of 918 participants. These studies were conducted in diverse ethnic populations, including Poland (Caucasian), Egypt (African), and Iran (Western Asian). All included studies demonstrated high methodological quality based on established criteria, including selection criteria, comparability of cases and controls in terms of study design and analytical approach, and completeness of genetic data. (Supplementary Table S2).

Table 1.

Characteristics of the Study Included in Meta-Analysis

First author	Year	Country	Ethnicity	Age	Genotyping method	Case/control	Genotype distribution			EAF (case/control)
First author	Year	Country	Ethnicity	Age	Genotyping method	Case/control	TT	TA	AA	EAF (case/control)
Suliga	2019	Poland	Caucasian	Adult	T-ARMS-PCR	108/110	43/43	56/50	9/17	0.34/0.38
Alnory	2016	Egypt	African	Adult	T-ARMS-PCR	100/100	38/25	51/59	11/16	0.37/0.45
Mehanna	2016	Egypt	African	Adult	T-ARMS-PCR	100/100	70/50	25/41	5/9	0.35/0.30
Hashemi	2012	Iran	Western Asian	Adult	T-ARMS-PCR	151/149	59/31	83/90	9/28	0.33/0.49

EAF, effective allele frequency; T-ARMS-PCR, tetra-primer amplification refractory mutation system-polymerase chain reaction.

Quantitative synthesis

The meta-analysis incorporated data from 459 cases and 459 controls. Among the included studies, Hashemi et al. contributed more weight to the analysis, while the rest of the studies had comparable contributions. However, their overall impact remained unaffected. Although the χ²-test for heterogeneity yielded a P-value > 0.10 and an I² statistic < 50%, a fixed-effects model was not employed due to the following considerations: (i) the Cochrane Library guidelines recommend fixed-effects models when I² is below 25%,¹⁹ and (ii) with a limited number of studies, I² may underestimate true heterogeneity. The analysis revealed that the effective allele-A was significantly more prevalent in controls, conferring a 37% reduction in the risk of MetS (OR: 0.63, 95% CI: 0.49–0.79, P = 0.0001) (Fig. 2). Given the limited number of studies, ethnic subgroup analysis was not performed. Consistent associations were observed across different genetic models, including the dominant (OR: 0.55, 95% CI: 0.37–0.82, P = 0.004), recessive (OR: 0.45, 95% CI: 0.29–0.70, P = 0.0004), homozygous (OR: 0.35, 95% CI: 0.20–0.59, P = 0.0001), and heterozygous (OR: 0.61, 95% CI: 0.40–0.93, P = 0.02) models (Fig. 2).

FIG. 2.

Association analysis between vaspin rs2236242 and Metabolic Syndrome (MetS).

Sensitivity analysis

To assess the robustness of our findings and address potential heterogeneity driven by the study of Suliga et al., we performed a leave-one-out sensitivity analysis. Notably, after excluding the Suliga et al. dataset, the heterogeneity of the meta-analysis was eliminated I² = 0%, while the protective association of the A-allele remained highly significant (OR: 0.57, 95% CI: 0.45–0.71, P < 0.00001). These findings indicate that the overall association is robust and not driven by the outlier study.

Publication bias

Visual inspection of the funnel plot, along with Egger’s regression test (P = 0.89) and Begg and Mazumdar’s rank correlation test (P = 0.50), provided no evidence of publication bias (Supplementary Fig. S2).

Discussion

Vaspin, a serine protease inhibitor predominantly expressed in visceral adipose tissue, has been implicated in insulin sensitivity regulation and inflammation, both of which are central to MetS pathogenesis.²⁰ The protective A allele may influence vaspin expression or function, potentially enhancing insulin signaling or attenuating pro-inflammatory pathways, though functional studies are required to validate this hypothesis. Prior investigations have also linked vaspin expression to obesity-related phenotypes and type 2 diabetes, supporting its broader metabolic relevance.⁵

To our knowledge, this is the first comprehensive meta-analysis investigating the association between the vaspin gene polymorphism rs2236242 and susceptibility to MetS. The findings of this study were derived from four selected independent case-control studies that involve 918 participants. The results clearly demonstrated that patients harboring allele-A of the rs2236242 had significantly reduced risk of MetS susceptibility by 37% as compared to the allele-T, indicating that this SNP has a protective effect against MetS. This association could be observed across multiple genetic models, dominant, recessive, homozygous, and heterozygous, further supporting that the vaspin gene polymorphism rs2236242 could be a potential genetic biomarker for MetS risk assessment.

The significant protective effect of the allele-A identified in this analysis is consistent with some existing literature emphasizing the beneficial metabolic effects associated with vaspin. Our findings agree with the two individuals studies that are included in this meta-analysis, which suggested that the A allele of rs2236242 is associated with a reduced risk of MetS.^13,21 These results support the hypothesis that the A allele may be metabolically beneficial, either by increased function of vaspin or improved insulin sensitivity. This notion was supported by²² that demonstrates that vaspin acts as a serine protease inhibitor, specifically inhibiting human kallikrein 7 (hk7), which is a protease that degrades insulin. Hence, it stabilizes insulin and improves insulin action. This mechanism of protease-inhibitory activity of vaspin offers a plausible cellular mechanism by which the A allele may confer protection against the MetS.

However, two other studies showed no significant association between the A allele of vaspin rs2236242 and the risk of developing MetS.^14,23 A study by¹⁴ that involves 200 Egyptian women has shown that the serum vaspin was significantly elevated among individuals with Mes. Still, no association has been shown between the vaspin rs2236242 genotypes and MetS. In this article, the author suggested some potential explanations such as the sample size of the population, the different ethnicity of the studied group, environmental factors, or even there’s interactions with other polymorphisms of the gene. They also suggested that larger studies are needed to validate these findings. Similarly, a study by²³ which involves the Polish cohort, had also found no statistically significant association between the vaspin rs2236242 genotypes and MetS. This study was identified as a potential outlier in our sensitivity analysis, possibly due to unique recombination patterns in that specific Caucasian subpopulation. Although the unadjusted model showed a trend toward the protective role for the AA genotype, the association is insignificant. In this study, the author acknowledged the small sample size and use of self-reported physical activity data may have influenced the statistical power and accuracy of their findings.

Other than that, there are some differences in the directionality of allele effects within single-country investigations. Study conducted by Abdel Ghany et al. (2017) and Amr and Mai (2019), demonstrated two Egyptian cohorts having discrepant effective allele frequencies (EAFs) for rs2236242 between T2DM cases and controls, which is possibly due to regional determinants of lifestyle or subpopulation structures within the country. Thus, further studies need to be conducted to rule out the possibilities.^24,25

According to the International Genome Sample Resource (IGSR, successor to the 1000 Genomes Project), rs2236242 is not present in the Phase 3 final variant set, although it appeared in earlier Phase 1 releases. This suggests that rs2236242 is not uniformly represented across modern reference panels and GWAS arrays, which may partially explain the limited evidence from large-scale GWAS. Therefore, this study was designed as a systematic review of published candidate-gene association studies rather than a de novo analysis of GWAS datasets.

Several limitations warrant consideration. First, the small number of eligible studies precluded subgroup analyses by ethnicity or sex, which could help identify population-specific effects. Second, heterogeneity metrics such as I² may be unreliable when few studies are included, potentially underestimating true between-study variance. Third, we acknowledge that component-specific genetic effects are biologically plausible and clinically important. However, only one of the eligible studies reported MetS components stratified by rs2236242 genotype. Therefore, we were unable to perform a component-level meta-analysis or calculate pooled mean ± SEM values, as quantitative synthesis requires data from multiple independent datasets. This reflects a common limitation of candidate gene association studies, which typically focus on the primary binary disease outcome rather than providing detailed genotype-stratified quantitative phenotypic data for individual metabolic traits. Fourth, the design of all the studies included inside the meta-analysis is cross-sectional, hence limits our ability to infer the causal effect of the vaspin rs2236242 polymorphism and MetS susceptibility.

Nonetheless, this study has been conducted using a rigorous methodological approach that includes a comprehensive literature search, stringent selection criteria, a detailed quality assessment of included studies, and robust sensitivity analyses that enhance the credibility of our findings. Importantly, despite the modest sample size and limited number of studies included, the results were robust across sensitivity analyses and showed no evidence of publication bias that further reinforces the reliability and credibility of the observed association between the rs2236242 polymorphism of vaspin and susceptibility of developing MetS. In addition, findings from this study are in the same direction with meta-analysis conducted on obesity, where vaspin rs2236242 is found to lower the risk of obesity but not in T2DM.¹²

Future studies should focus on validating these associations in larger, multi-ethnic cohorts with standardized phenotyping, as well as investigating the mechanistic consequences of rs2236242 polymorphism on vaspin expression and metabolic function, as there are variability in allele frequencies and genetic backgrounds among different populations. Moreover, genome-wide interaction studies and epigenetic analyses could help elucidate gene–environment interplay in MetS development. For instance, a study by Suliga et al. (2019) suggests that physical activity, particularly walking more than 60 min per day, may reduce the risk of MetS among individuals with the TA or AA genotype of vaspin rs2236242.²³ To add on, longitudinal studies are also essential to clarify the temporal sequence and confirm whether the genetic variants of the vaspin gene do influence the MetS development.

Conclusion

In conclusion, this meta-analysis provides the first aggregated evidence that the vaspin rs2236242 A allele confers a protective effect against MetS. These findings support a potential role for vaspin rs2236242 in MetS susceptibility and highlight the need for further genetic and functional investigations to help in early identification of individuals that have a higher risk of developing MetS. Morever, vaspin rs2236242 could be a good genetic biomarker for MetS risk assessment in the future and aid in the advancement of precision metabolic medicine.

Authors’ Contributions

W.-Y.L.: Writing—review and editing, writing—original draft, conceptualization, data curation, formal analysis. A.E.A.: Writing—review and editing, writing—original draft, conceptualization, data curation, formal analysis. Y.-F.P.: Writing—review and editing, conceptualization. R.M.: Review and editing. R.-X.N.: Writing—review and editing. S.M.Z.: Writing—review and editing, conceptualization, supervision. All authors approved the final version of the article.

Footnotes

Acknowledgments

The work was not supported by any external funding.

Original Work Contribution

This contribution represents original work that has not been previously published or simultaneously submitted for publication elsewhere.

Author Contribution and Approval

All authors contributed to the conception and design of the article and interpreting the relevant literature. All authors were involved in writing the article or revising it for intellectual content. The article has been read and approved by all the authors who agree to be accountable for all aspects of the work. All ICMJE conditions have been met.

Funding Information

No funding was received for this article.

Supplemental Material

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Association of Vaspin rs2236242 with Metabolic Syndrome: A Meta-Analysis of Case–Control Studies