Mechanism of Gut Microbiota Dysbiosis in Insulin Resistance Polycystic Ovary Syndrome

INTRODUCTION: Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder associated with insulin resistance, hyperandrogenism, and infertility. Gut microbiota dysbiosis is suspected to play a significant role in the pathogenesis of PCOS through the gut-brain-gonad axis, an axis that remains incompletely understood. METHODS: , levels of Zonulin, Short Chain Fatty Acids (SCFAs), Insulin-Like Growth Factor-1 (IGF-1), and ovarian follicle count in a rat model of PCOS with insuline resistance, which in this study devided into 2 groups, control and treatment group, consist of 20 rats each. This experimental study employed an SEM-PLS approach to assess the relationships among microbiota, inflammation, metabolism, and ovarian function variables in an insulin-resistant PCOS rat model with insulin resistance. RESULTS: The results showed decreases in Lactobacillus sp., SCFAs, and ovarian follicle counts, along with an increase in IGF-1 levels in PCOS model rats. DISCUSSION: was linked to lower SCFA levels, which influenced IGF-1 and negatively affected ovarian follicle development; (2) Inflammation/Insulin Resistance Pathway: The model established a statistically significant cascade where PCOS induction was strongly associated with Zonulin (β = -0.717), which then positively predicted HOMA-IR (β = 0.630), and HOMA-IR, in turn, strongly predicted IGF-1 (β = 0.662), defining the mechanism as PCOS → Zonulin → HOMA-IR → IGF-1. CONCLUSION: The dysbiosis mechanism involving gut microbiota in this study's model includes PCOS, Zonulin, HOMA-IR, and IGF-1, as these variables demonstrated statistically significant relationships.