Objective: This study investigates the insulin resistance (IR) status in patients with endometrial polyps (EP) and analyzes its correlation with the endometrial expression of insulin receptor (InR), insulin-like growth factor-1 receptor (IGF-1R), and insulin receptor substrate-1 (IRS-1) and IRS-2, so as to preliminarily explore the potential molecular association between EP and IR.
Methods: A total of 170 patients who underwent hysteroscopy due to abnormal uterine bleeding or ultrasonic evidence of intrauterine abnormal echoes or space-occupying lesions were divided into Polyp group (endometrial polyps, n=84) and Control group (normal endometrium, n=86) based on endometrial pathology results. Clinical data and IR-related indicators [fasting plasma glucose (FPG), fasting insulin (FIN), and homeostasis model assessment-insulin resistance index (HOMA-IR)] were compared between the two groups. Immunohistochemistry was performed to compare the expression differences of InR, IGF-1R, IRS-1, and IRS-2 in endometrial tissues.
Results: Patients with endometrial polyps had significantly elevated FIN and HOMA-IR compared to the control group; the incidence of IR was slightly higher in the polyp group without statistical significance. There were no statistically significant differences in the expression of InR, IGF-1R, IRS-1, and IRS-2 among endometrial polyps, peri-polyp endometrium, and normal endometrium. No significant inter-group differences of the four target proteins were observed between proliferative and secretory phases in either group. Within both the polyp and control cohorts, endometrial expression of the four molecules showed no obvious difference between insulin-resistant (IR subgroup) and non-insulin-resistant (NIR subgroup) patients.
Conclusion: Patients with endometrial polyps tend to exhibit insulin-resistant metabolic profiles. However, the expression levels of InR, IGF-1R, IRS-1 and IRS-2 in polyp tissue show no significant difference compared with adjacent peri-polyp endometrium and normal endometrium. Combined with previous research focusing on downstream insulin signaling cascades, we hypothesize that the pathogenesis of endometrial polyps may be associated with abnormalities in post-insulin-receptor signaling pathways; further mechanistic experiments detecting downstream signaling proteins are required to verify this hypothesis.