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Additionally, these agents may influence the advancement of atherosclerosis through their anti-inflammatory impact on endothelial cells, their capacity to diminish smooth muscle cell proliferation, and their ability to attenuate the pro-inflammatory responses of macrophages [67]

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Attributed to the selective IR paradox, compensatory hyperinsulinemia can amplify hyperandrogenism via several mechanisms: (i) cross-activation of insulin and/or IGF-1 receptors, which enhances LH-mediated expression of key steroidogenic enzymes (e.g., CYP17A1) in ovarian theca cells and increases androgen synthesis