Abstract
Objective: To Conduct a systematic review of the literature in order to clarify and discuss the effects of SNP rs7903146 in the TCF7L2 gene and predisposition to Metabolic Syndrome (MS) modulation by dietary factors such variant. Methods: We performed a review of the literature in a systematic way from original studies between 2000 and 2013, found in Medline, PubMed, Wiley library, SciELO, ScienceDirect, Springer link, The University of Adelaide, DeepDyve, Cambridge journals. Results: The clinical trials reported in this study indicated a significant correlation between the risk allele of rs7903146 polymorphism and pathophysiological characteristics of MS, with the most consistent findings with changes in glucose homeostasis, insulin metabolism and atherogenic dyslipidemia for each study population. Conclusions: This review highlights the scientific evidence for rs7903146 polymorphism as one of the etiologic basis for MS. However, demonstrates the need for greater standardization of investigations, to reduce possible population variables with potential influence on the results, such as environmental factors and genetic heterogeneity.
Highlights
Of increasing prevalence, in addition to multiple etiologies and not fully explained, the Metabolic Syndrome (MS) is a complex disorder pointed as a result of the combination of several factors, such as overweight/obesity, sedentary lifestyle and poor eating habits.The MS leads to an increase in cardiovascular risk, clinically identified by significant increases in blood pressure, fasting blood glucose levels, measures of waist circumference and serum concentrations of triglycerides (TG), which may be accompanied by a reduction in the levels of high-density lipoproteins (HDL).(1) It is a global epidemic, affecting a quarter of the adult population worldwide
Many of genetic variants identified so far are characterized as Single Nucleotide Polymorphisms (SNP), which represent distinct changes in the sequence human genome responsible for triggering of various physiological disorders.(1,2,3) Different from the most classic mutations, the SNPs present a higher frequency in the population and originate from a point mutation, representing the change of a nitrogen base in the DNA sequence.(1)
Inclusion criteria were: clinical studies, preferably with controlled and randomized approach, studying the correlation between the polymorphism rs7903146 in Transcription Factor 7-Like 2 (TCF7L2) gene and comorbidities associated with Metabolic Syndrome, it was an inclusion criteria the demonstration that genotypes were in HardyWeinberg equilibrium, to exclude possible genotypic errors
Summary
In addition to multiple etiologies and not fully explained, the Metabolic Syndrome (MS) is a complex disorder pointed as a result of the combination of several factors, such as overweight/obesity, sedentary lifestyle and poor eating habits. Many of genetic variants identified so far are characterized as Single Nucleotide Polymorphisms (SNP), which represent distinct changes in the sequence human genome responsible for triggering of various physiological disorders.(1,2,3) Different from the most classic mutations, the SNPs present a higher frequency in the population (higher than the 1%) and originate from a point mutation, representing the change of a nitrogen base in the DNA sequence.(1). The present study aims to review recent experimental studies on physiological effects of single nucleotide polymorphisms, the polymorphism rs7903146 in TCF7L2 gene and its role in the predisposition of Metabolic Syndrome Another focus of the study was to analyze the results of studies that have evaluated promising gene-nutrient interactions modulating the effect of this polymorphism
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