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Most findings come from early-stage or limited human studies, which provide insight into mechanisms but do not establish consistent clinical outcomes across populations
Such modifications then activate NF-B that is involved in the expression of proinflammatory mediators such as TNF and IL-6, 343,344 and that induces key steroidogenic molecules, like CYP11A1, CYP17A1 and StAR, leading to further aggravation of hyperandrogenemia
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