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
They are essential for synaptic transmission, as they allow ions to flow in response to chemical signals released by neighboring neurons, facilitating communication within neural networks ( 4
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