When examining the whole cohort or A group separately, we saw that the CAGs enriched by the intervention were negatively correlated with the disease phenotypes, such as the LH/FSH ratio, testosterone, metabolic parameters including FINS and homeostasis model assessment-insulin resistance (HOMA-IR), α-AGP, leptin, and orexin, and positively correlated with adiponectin and spexin, while the CAGs inhibited had an opposite trend (Figures 6A, B). The gene discussed is PLOD1; the disease is Insulin resistance.