Why the study?
While endogenous estrogen is cardioprotective in healthy premenopausal women, animal models suggest detrimental effects on vascular function in diabetes, prompting investigation into the role of endogenous estradiol in women with type 1 diabetes.
Does endogenous estradiol contribute to vascular endothelial dysfunction in premenopausal women with type 1 diabetes?
Does endogenous estradiol contribute to vascular endothelial dysfunction in premenopausal women with type 1 diabetes?
Endogenous estradiol appears to increase oxidative stress and worsen endothelial function in premenopausal women with type 1 diabetes, contrasting with its protective effects in healthy women.
Estradiol-associated endothelial impairment in premenopausal T1D may warrant monitoring; leaves open whether hormone modulation alters outcomes.
BACKGROUND: Endogenous estrogen is cardio-protective in healthy premenopausal women. Despite this favorable action of estrogen, animal models depict a detrimental effect of estradiol on vascular function in the presence of diabetes. The present study sought to determine the role of endogenous estradiol on endothelial function in women with type 1 diabetes. METHOD: = 8.9 ± 2.1%). RESULTS: Overall, estradiol was significantly increased during the LF phase compared to M in both type 1 diabetes (Δestradiol = 75 ± 86 pg/mL) and controls (Δestradiol = 71 ± 76 pg/mL); however, an increase in TBARS was only observed in patients with type 1 diabetes (ΔTBARS = 3 ± 13 µM) compared to controls (ΔTBARS = 0 ± 4 µM). FMD was similar (p = 0.406) between groups at M. In addition, FMD increased significantly from M to the LF phase in controls (p = 0.024), whereas a decrease was observed in type 1 diabetes. FMD was greater (p = 0.015) in patients using HBC compared to those not on HBC, independent of menstrual cycle phase. CONCLUSION: Endogenous estradiol increases oxidative stress and contributes to endothelial dysfunction in women with diabetes. Additionally, HBC use appears to be beneficial to endothelial function in type 1 diabetes.
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Simon et al. (2023) studied this question.
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