Insulin resistance (IR) is an important pathological feature of polycystic ovary syndrome (PCOS), with an incidence rate of up to 85%, which seriously affects the patient's fertility, quality of life, and offspring health, but the mechanism is unknown. The adaptor protein LNK is closely related to metabolic diseases. Our exome sequencing has found that the mutation rate of LNK gene in patients with PCOS and IR is high. Studies have found that LNK can affect adipose inflammation and impair glucose tolerance. Whether LNK is related to fat metabolism is worth further study. Our previous research found that: LNK expression was significantly increased in adipose tissue of patients with PCOS and IR. Knockout of LNK in PCOS IR model mice can reduce serum triglycerides, free fatty acids, high-sensitivity C-reactive protein levels and reduce fatty liver occurrence, which indicates that LNK has a mitigating effect on IR. Mechanism studies have shown that LNK knockout can upregulate the glucose transporter Glut4, also LNK and insulin receptor substrate IRS-1 can form protein complexes. Based on the above research basis, we propose the following scientific hypothesis: LNK in adipose tissue can regulate insulin signaling pathway by binding to IRS-1, downregulate Glut4, and participate in PCOS IR occurrence. This project intends to clarify the specific mechanism by which LNK regulates glucose transport and participate in IR in combination with clinical specimens, animal models and cell experiments, and provide scientific basis for LNK as a potential therapeutic target for PCOS IR.

Inclusion Criteria:

• Patients with polycystic ovary syndrome who meet the 2003 Rotterdam criteria

Exclusion Criteria:

• Do not meet the diagnostic criteria for polycystic ovary syndrome

Patients with polycystic ovary syndrome who met the 2003 Rotterdam criteria were divided into insulin resistance group and non-insulin resistance group