Diabetic patients with heterogeneous insulin levels and/or poor glycemic control in the body can lead to dysregulation of hormone secretion in the hypothalamic-pituitary-ovarian axis, abnormal follicle recruitment and egg development, resulting in impaired reproductive capacity. 1. Hypogonadotropic hypogonadism In insulin-deficient diabetic patients, low insulin levels can lead to decreased hypothalamic kisspeptin protein expression. Since kisspeptin has the function of stimulating the secretion of gonadotropin-releasing hormone (GnRH), insulin deficiency may reduce the secretion of GnRH, which further leads to insufficient secretion of both folliculopoietin/luteinizing hormone (FSH/LH), resulting in hypogonadotropic hypogonadism. Supplementation with exogenous insulin can correct this hormone level abnormality. 2, hyperandrogenism and polycystic ovaries In diabetic patients who need subcutaneous insulin injections, the insulin level in peripheral tissues is higher than in the physiological state because exogenous insulin enters the body circulation directly without the clearance effect of the liver. In addition, some patients with type 2 diabetes or abnormal glucose tolerance have high endogenous insulin levels due to insulin resistance. The excessive levels of endogenous and exogenous insulin caused by the above two reasons can firstly promote the secretion of testosterone and androstenedione by follicular membrane cells leading to hyperandrogenemia; secondly the combined effect of insulin and FSH can stimulate granulosa cells to secrete estrogen and promote follicle recruitment and growth, resulting in the manifestation of polycystic ovaries. Unlike non-diabetic polycystic ovary syndrome, insulin can promote follicle maturation in synergy with gonadotropins. 3. Decreased ovarian reserve and egg apoptosis Poorly controlled diabetes leads to elevated blood glucose. On one hand, hyperglycemia leads to an increase in late glycosylation end products and their receptors, which can affect egg development and cause egg apoptosis and decreased ovarian reserve function. On the other hand, glucotoxicity aggravates insulin resistance, resulting in excessive secretion of endogenous insulin or increased dosage of exogenous insulin, thus exposing the ovary to a hyperinsulinemic environment.