Vascular effects of estrogen in type II diabetic postmenopausal women

Kwang Kon Koh, Moon Ho Kang, Dong Kyu Jin, Seon Kyu Lee, Jeong Yeal Ahn, Hee Young Hwang, Seong Hee Yang, Dae Sung Kim, Tae Hoon Ahn, Eak Kyun Shin

Research output: Contribution to journalArticle

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Abstract

OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic post-menopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 ± 23% (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 ± 16% (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 ± 24%, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 ± 48% and lower glycosylated hemoglobin levels by 3 ± 13% (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 ± 75% vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5%. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 ± 46% and 5 ± 34%, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 ± 31% (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.

Original languageEnglish (US)
Pages (from-to)1409-1415
Number of pages7
JournalJournal of the American College of Cardiology
Volume38
Issue number5
DOIs
StatePublished - Nov 1 2001
Externally publishedYes

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Blood Vessels
Estrogens
Placebos
Thromboplastin
HDL Cholesterol
Conjugated (USP) Estrogens
E-Selectin
Vascular Cell Adhesion Molecule-1
Chemokine CCL2
Plasminogen Activator Inhibitor 1
Matrix Metalloproteinase 9
Hyperemia
Glycosylated Hemoglobin A
Intercellular Adhesion Molecule-1
LDL Lipoproteins
LDL Cholesterol
Cross-Over Studies
Lipoproteins
Nitric Oxide
Triglycerides

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Vascular effects of estrogen in type II diabetic postmenopausal women. / Koh, Kwang Kon; Kang, Moon Ho; Jin, Dong Kyu; Lee, Seon Kyu; Ahn, Jeong Yeal; Hwang, Hee Young; Yang, Seong Hee; Kim, Dae Sung; Ahn, Tae Hoon; Shin, Eak Kyun.

In: Journal of the American College of Cardiology, Vol. 38, No. 5, 01.11.2001, p. 1409-1415.

Research output: Contribution to journalArticle

Koh, KK, Kang, MH, Jin, DK, Lee, SK, Ahn, JY, Hwang, HY, Yang, SH, Kim, DS, Ahn, TH & Shin, EK 2001, 'Vascular effects of estrogen in type II diabetic postmenopausal women', Journal of the American College of Cardiology, vol. 38, no. 5, pp. 1409-1415. https://doi.org/10.1016/S0735-1097(01)01566-2
Koh, Kwang Kon ; Kang, Moon Ho ; Jin, Dong Kyu ; Lee, Seon Kyu ; Ahn, Jeong Yeal ; Hwang, Hee Young ; Yang, Seong Hee ; Kim, Dae Sung ; Ahn, Tae Hoon ; Shin, Eak Kyun. / Vascular effects of estrogen in type II diabetic postmenopausal women. In: Journal of the American College of Cardiology. 2001 ; Vol. 38, No. 5. pp. 1409-1415.
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abstract = "OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic post-menopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 ± 23{\%} (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 ± 16{\%} (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 ± 24{\%}, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 ± 48{\%} and lower glycosylated hemoglobin levels by 3 ± 13{\%} (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 ± 75{\%} vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5{\%}. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 ± 46{\%} and 5 ± 34{\%}, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 ± 31{\%} (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.",
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T1 - Vascular effects of estrogen in type II diabetic postmenopausal women

AU - Koh, Kwang Kon

AU - Kang, Moon Ho

AU - Jin, Dong Kyu

AU - Lee, Seon Kyu

AU - Ahn, Jeong Yeal

AU - Hwang, Hee Young

AU - Yang, Seong Hee

AU - Kim, Dae Sung

AU - Ahn, Tae Hoon

AU - Shin, Eak Kyun

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N2 - OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic post-menopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 ± 23% (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 ± 16% (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 ± 24%, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 ± 48% and lower glycosylated hemoglobin levels by 3 ± 13% (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 ± 75% vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5%. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 ± 46% and 5 ± 34%, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 ± 31% (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.

AB - OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic post-menopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 ± 23% (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 ± 16% (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 ± 24%, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 ± 48% and lower glycosylated hemoglobin levels by 3 ± 13% (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 ± 75% vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5%. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 ± 46% and 5 ± 34%, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 ± 31% (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.

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