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ENDOTHELIAL FUNCTION

Vascular effects of estrogen in type II diabetic postmenopausal women

Kwang Kon Koh, MD, PhD, FACC^*,*, Moon Ho Kang, MD, PhD, Dong Kyu Jin, MD, PhD^*, Seon-Kyu Lee, MD, Jeong Yeal Ahn, MD, PhD, Hee Young Hwang, MD, Seong Hee Yang, MD^||, Dae Sung Kim, MD, PhD^¶, Tae Hoon Ahn, MD, PhD^* and Eak Kyun Shin, MD, PhD^*

^* Department of Cardiology, Inchon, South Korea
Endocrinology and Metabolism, Inchon, South Korea
Clinical Pathology, Inchon, South Korea
Radiology, Inchon, South Korea
^|| Menopause Clinic, Inchon, South Korea
^¶ Preventive Medicine (Biostatistics), Gachon Medical School, Incheon, South Korea

Manuscript received January 5, 2001; revised manuscript received June 11, 2001, accepted July 11, 2001.

^* Reprint requests and correspondence: Dr. Kwang Kon Koh, Director, Vascular Medicine and Atherosclerosis Unit, Division of Cardiology, Gil Heart Center, Gachon Medical School, 1198 Kuwol-Dong, Namdong-Gu, Incheon, North Korea 405-760
kwangk{at}ghil.com

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 postmenopausal 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.

Abbreviations and Acronyms   CAD = coronary artery disease   CEE = conjugated equine estrogen   CI = confidence interval   ELISA = enzyme-linked immunosorbent assay   HERS = Heart and Estrogen/progestin Replacement Study   HDL = high-density lipoprotein   ICAM-1 = intercellular adhesion molecule-1   LDL = low-density lipoprotein   MCP-1 = monocyte chemoattractant protein-1   MMP-9 = matrix metalloproteinase-9   mRNA = messenger ribonucleic acid   NO = nitric oxide   PAI-1 = plasminogen activator inhibitor-1   TF = tissue factor   VCAM-1 = vascular cell adhesion molecule-1

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