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. 2023 Jan 23;14:1096187. doi: 10.3389/fendo.2023.1096187

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Copyright © 2023 Gurule, Sustaita-Monroe, Padmanabhan and Cardoso

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A schematic representation of the neuroendocrine alterations seen in the sheep model of PCOS phenotype. Imbalances in KNDy neuron peptide and receptor expression in the hypothalamus disrupt GnRH tonic secretion and responsiveness to steroid hormone feedback systems regulating reproductive cyclicity. Puberty attainment is altered due to decreased responsiveness to the estradiol (E2) inhibitory feedback. Reduced sensitivity to the progesterone (P4) negative feedback and increased pituitary sensitivity to GnRH result in LH hypersecretion and imbalance of the LH : FSH ratio, which in turn impairs follicular development and ovarian steroidogenesis. Impairments in the estradiol positive feedback mechanism result in disrupted (delayed and reduced amplitude) preovulatory surge of LH surge, thus compromising ovulatory capacity. Created with BioRender.com.