This study investigates the mechanism behind the elevated luteinizing hormone (LH)/follicle-stimulating hormone (FSH) ratio in lean polycystic ovary syndrome (PCOS) patients. The research focuses on neuroendocrine pathways, particularly the roles of kisspeptin, neurokinin B (NKB), dynorphin, and anti-Müllerian hormone (AMH). The study involved 110 lean PCOS patients and measured various hormonal and metabolic parameters. Bivariate and path analyses were conducted to explore the relationships between these variables. The findings indicate a negative association between dynorphin and kisspeptin levels, while NKB levels were not significantly associated with kisspeptin. AMH was positively correlated with the LH/FSH ratio, suggesting its role in neuroendocrine regulation in lean PCOS. Path analysis revealed that AMH acts as an intermediary variable between HOMA-IR and FAI, influencing the LH/FSH ratio. Additionally, a significant positive correlation was found between dynorphin and the LH/FSH ratio, while no significant association was found between kisspeptin and the LH/FSH ratio. The study proposes a novel mechanism for the elevated LH/FSH ratio in lean PCOS, involving disruptions in the negative feedback mechanism of estradiol and progesterone, increased kisspeptin secretion from KNDy neurons, and the direct effect of dynorphin on GnRH neurons. These factors contribute to increased LH secretion and altered LH/FSH ratios. AMH levels were also found to influence the LH/FSH ratio by affecting GnRH neurons and suppressing aromatase enzyme expression in granulosa cells. The study highlights the importance of AMH and dynorphin as potential therapeutic targets in the management of lean PCOS. Further research is needed to explore the therapeutic potential of these factors in lean PCOS patients. The findings suggest that targeting these pathways could lead to more effective treatments for lean PCOS, particularly in addressing the neuroendocrine disturbances associated with the condition.This study investigates the mechanism behind the elevated luteinizing hormone (LH)/follicle-stimulating hormone (FSH) ratio in lean polycystic ovary syndrome (PCOS) patients. The research focuses on neuroendocrine pathways, particularly the roles of kisspeptin, neurokinin B (NKB), dynorphin, and anti-Müllerian hormone (AMH). The study involved 110 lean PCOS patients and measured various hormonal and metabolic parameters. Bivariate and path analyses were conducted to explore the relationships between these variables. The findings indicate a negative association between dynorphin and kisspeptin levels, while NKB levels were not significantly associated with kisspeptin. AMH was positively correlated with the LH/FSH ratio, suggesting its role in neuroendocrine regulation in lean PCOS. Path analysis revealed that AMH acts as an intermediary variable between HOMA-IR and FAI, influencing the LH/FSH ratio. Additionally, a significant positive correlation was found between dynorphin and the LH/FSH ratio, while no significant association was found between kisspeptin and the LH/FSH ratio. The study proposes a novel mechanism for the elevated LH/FSH ratio in lean PCOS, involving disruptions in the negative feedback mechanism of estradiol and progesterone, increased kisspeptin secretion from KNDy neurons, and the direct effect of dynorphin on GnRH neurons. These factors contribute to increased LH secretion and altered LH/FSH ratios. AMH levels were also found to influence the LH/FSH ratio by affecting GnRH neurons and suppressing aromatase enzyme expression in granulosa cells. The study highlights the importance of AMH and dynorphin as potential therapeutic targets in the management of lean PCOS. Further research is needed to explore the therapeutic potential of these factors in lean PCOS patients. The findings suggest that targeting these pathways could lead to more effective treatments for lean PCOS, particularly in addressing the neuroendocrine disturbances associated with the condition.