Abstract
BackgroundMetabolic syndrome is a cluster of factors associated with an increased risk of developing type 2 diabetes mellitus (T2D) and coronary artery disease (CAD). It is a complex disorder resulting from the interaction between various environmental factors and genetic susceptibility. The somatostatin (SST) gene has been shown to regulate a wide range of functions, particularly in energy homeostasis. In addition, low levels of SST have been reported to have effects on the progression of metabolic syndrome components. The aim of this study was therefore to evaluate the association between polymorphic T sequences in the promoter of the SST gene and metabolic syndrome expression.MethodsWe studied 1725 French-Canadian subjects from a founder population selected on the basis of having a positive family history of dyslipidemia, CAD or T2D. The analysis were performed on four groups created according to the poly T polymorphism length in the 5′ flanking promoter region of SST. Anova, Ancova and logistic regression models and Chi 2 analyses were used to evaluate the association between the poly T polymorphisms and metabolic syndrome components expression.ResultsAnalyses showed that means, frequencies and odds ratio of metabolic syndrome components expression increase as the number of poly-T repeats in the promoter region of SST increases. Women exhibit more significant differences than men. However, the trends are the same in both genders and differences for most of the components are significant in the entire sample.ConclusionThose results suggest that the poly T polymorphisms in the SST promoter region may influence several metabolic processes implicated in metabolic syndrome expression. More analyses are needed to document the mechanisms that could underlie genetic regulation effect of SST on metabolic syndrome components and to clarify its specific role.
Highlights
Metabolic syndrome is a cluster of factors associated with an increased risk of developing type 2 diabetes mellitus (T2D) and coronary artery disease (CAD)
It has been estimated that people with metabolic syndrome are at twice the risk of developing coronary artery disease (CAD), compared with those without the syndrome, and experience a five-fold increased risk of type 2 diabetes (T2D) [1]
T2D was defined according to the World Health Organization criteria as a 2-h glucose concentration > 11.1 mmol/L following a 75 g oral glucose load, whereas a normal glucose tolerance state was characterized as a 2-h glucose concentration below 7.8 mmol/L
Summary
Metabolic syndrome is a cluster of factors associated with an increased risk of developing type 2 diabetes mellitus (T2D) and coronary artery disease (CAD). It is a complex disorder resulting from the interaction between various environmental factors and genetic susceptibility. Metabolic syndrome is a cluster of interrelated common clinical disorders occurring together more often than by chance alone. It includes hyperglycaemia, hypertension, elevated triglyceride (TG) levels, low high-density lipoprotein (HDL) cholesterol levels and central obesity. Numerous genome-wide association studies (GWAS) have been carried out for many common diseases, including metabolic syndrome and related covariables [3, 4]. Combined with functional studies and gene-environment interaction analyses, the mapping of gene networks associated with complex diseases, such as metabolic syndrome, may be essential to unveiling their aetiology and biological mechanisms [4]
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