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Despite evidence that estrogens and insulin are related to type 1 endometrial carcinoma (EC), their synergistic role has not been analyzed. Here, we investigated how estrogens cooperate with insulin to promote type 1 EC progression. We examined the clinical significance of serum estrogen and insulin levels using type 1 EC patients and control subjects. Univariate and multivariate logistic regression analyses for total, premenopausal, and postmenopausal subjects were performed. Type 1 EC risk was evaluated with respect to estrone, estradiol, and insulin levels based on odds ratios (ORs) using stratified data. Cell growth in vitro and in vivo, effects of insulin and estradiol on apoptosis and cell cycle distribution were measured after estradiol and insulin stimulation. Estrone and insulin concentrations were significantly high in type 1 EC patients and retained positive associations with type 1 EC after adjustment for BMI, WHR, diabetes, and hypertension. The odds ratio was significantly high for type 1 EC patients with higher levels of estrone/estradiol and insulin than for patients with higher levels of either estrone/estradiol or insulin, suggesting that estrogen and insulin play a synergistic role in type 1 EC carcinogenesis and progression. Compared to EC cells and cell-based xenografts treated with estradiol or insulin alone, those treated with estradiol and insulin exhibited stronger stimulation. Estrogen and insulin play synergistic roles in type 1 EC carcinogenesis and progression, extending our understanding of EC risks.

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The relationship between polycystic ovary syndrome (PCOS) and subclinical atherosclerosis remains unclear. We performed a comprehensive systematic review and meta-analysis to evaluate the effect of PCOS on functional and structural markers of subclinical atherosclerosis as measured by carotid intima-media thickness (cIMT), flow-mediated vasodilation (FMD), nitroglycerin-mediated vasodilation (NMD), pulse wave velocity (PWV), and coronary artery calcium (CAC). Standard mean differences (SMDs) or odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated. Ninety-six articles involving 5550 PCOS patients and 5974 controls were included. Compared with controls, PCOS patients showed significantly thicker cIMT (SMD (95% CI) = .587 (.398, .776), P < .001), lower FMD (SMD (95% CI) = −.649 (−.946, −.353), P < .001) and NMD (SMD (95% CI) = −.502 (−.686, −.317), P < .001), as well as higher PWV (SMD (95% CI) = .382 (.019, .746), P = .039), and increased CAC incidence (OR (95% CI) = 2.204 (1.687, 2.879), P < .001). When analyzing subgroups by age and body mass index (BMI), results were still significant ( P < .05) except for PWV in the BMI subgroup. There was no significant result on sensitivity analysis, and Begg’ test or Egger’s test. PCOS contributes to subclinical atherosclerosis, resulting in functional and structural changes in cIMT, FMD and NMD, PWV, and CAC incidence.