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Hyperaldosteronism is associated with impaired vascular reactivity, and it has been shown that aldosterone induces a G6PD-deficient phenotype to impair endothelial function, and aldosterone antagonism or gene transfer of G6PD improves vascular reactivity [9]

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Because IGF-1 is normally found at low levels in MetS and T2D, maybe because of insulin cessation to inhibit IGFBP-1 production by the liver and because of decreased liver IGF-1 secretion by insulin stimulation, as insulin resistance prevails in the liver