Correlation between Insulin Resistance and Steroid Endometrial Receptors, KI-67 and BCL-2 after Menopause

Abstract

Introduction: After menopause, the distribution of weight gain and fat deposits may be altered, with a predominance of abdominal fat. This fat has been correlated with the appearance of metabolic and neoplastic diseases. In the endometrium, proliferative lesions may be mediated by steroid endometrial receptors. The aim of this study was to evaluate the association between steroid receptors, proliferation and apoptotic factors and the presence of insulin resistance (IR) in women after menopause. Methods: The experimental design was an observational cross-sectional study of 85 postmenopausal women. The average age of the women was of 56.8 years (SD= 6.5) with an average menopause period of 81.5 months (SE = 6.39). An atrophic endometrial specimen was collected from asymptomatic, post-menopausal women. An endometrial sample was collected and the expression of estrogen (ER), progestogen (PR) and insulin growth factor-1 (IGF-1R) receptors, as well as Ki-67 and Bcl-2, was evaluated and their correlation with IR was assessed. Results: There was marked expression of ER (94.1%), PR (80%) and IGF-1R (78.8%) in endometrial glands. There was a correlation between the HOMA-IR index and stromal ER (p=0.378) and PR (p=0.0083) expression, as well as a correlation between ER and the expression of Ki-67 (p=0.253) and Bcl-2 (p<0.05). Conclusion: These results suggest that IR may stimulate the expression of endometrial receptors, thereby contributing to an increased risk of endometrial proliferative diseases.

Insulin Resistance and Endometrial Cancer: Emerging Role for microRNA

“…Furthermore, an in vitro study showed that insulin directly stimulates aromatase activity in both endometrial glands and stroma, which strongly suggests that hyperinsulinemia caused by IR predisposes to EC by enhancing endogenous endometrial estrogen production [104]. Work by Galvão Wolff et al indicated that IR stimulates endometrial expression of ERs and progesterone receptors (PRs), thereby contributing to the increased occurrence of endometrial proliferative lesions [105].…”