Overweight, But Not Hypertension, Is Associated with SAH Polymorphisms in Caucasians with Essential Hypertension
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<B>The gene <I>SAH</I> (chromosome 16p12.3) is of interest in the etiology of human hypertension. In Caucasians a <I>Pst</I>I restriction fragment length polymorphism (RFLP) of <I>SAH</I> has been correlated with body weight in individuals with hypertension. To extend this finding we carried out a case-control study of several recently identified polymorphisms in <I>SAH</I>: 1) an insertion/deletion of TTTAA at nucleotide -1037 in the promoter; 2) an insertion/deletion of two <I>Alu</I> like sequences in intron 1; and 3) an A→G variant in intron 12 located 7 bp upstream from exon 13. Subjects were 121 hypertensives with 2 hypertensive parents and 178 normotensives whose parents were both normotensive. All were Anglo-Celtic Caucasians and 51% of the hypertensives were overweight (body mass index (BMI)>25 kg/m<SUP>2</SUP>). The <I>SAH</I> promoter and intron 1 variants, but not the intron 12 or <I>Pst</I>I RFLP, were in linkage disequilibrium (LD) (<I>D′</I>=100%, <I>p</I> <0.001). We found no association between any of the polymorphisms and hypertension. However, the frequency of the minor allele of the intron 1 polymorphism (0.20) was higher in overweight than in normal weight hypertensives (0.07) (<I>p</I> =0.013). This association was supported by the weak tracking of plasma lipid variables with this allele (<I>p</I> values=0.01-0.04), although these lost their statistical significance after correction for multiple comparisons. In conclusion, the present data offers support for variation in <I>SAH</I> having a role in predisposition to overweight in hypertensives. (<I>Hypertens Res</I> 2003; 26: 591-595)</B>
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