Oral but not transdermal estrogen replacement therapy changes the composition of plasma lipoproteins

Vrablík, M.; Fait, T; Kovář, J.; Poledne, R.; Češka, R.

doi:10.1016/j.metabol.2008.03.012

Cited by 42 publications

(21 citation statements)

References 45 publications

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“…14 C] estradiol, [4][5][6][7][8][9][10][11][12][13][14] C]NEC-127 estradiol with a specific activity of 54.1 mCi/mmol, was obtained from DuPont NEN (lot number 3188-151SP; Boston, MA, USA) and was kept at 4°C until it was used. The dose was composed of estradiol 10% and vehicle 90% to include ethanal 80% and propylene glycol (PEG) 20%.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

In vitrohuman topical bioactive drug transdermal absorption: estradiol

Xing¹,

Hui²,

Zhong³

et al. 2009

Cutaneous and Ocular Toxicology

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Section: Methodsmentioning

confidence: 99%

“…Oral estradiol induces antiatherogenic changes in endothelium-dependent vasodilatation and lipid concentrations (7). Compared with transdermal therapy, oral therapy changes negatively the composition of plasma lipoproteins (8).…”

Section: Introductionmentioning

confidence: 99%

In vitrohuman topical bioactive drug transdermal absorption: estradiol

Xing¹,

Hui²,

Zhong³

et al. 2009

Cutaneous and Ocular Toxicology

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“…On the other hand, estradiol treatment could attenuate the above changes, which were consistent with previous studies. 32,33 However, the changes were not significant compared with the aforementioned studies, which might be due to the fact that the E2 was given intramuscularly rather than orally. Studies showed that hyperlipidemia could induce senescence of EPCs, which further resulted in cellular dysfunction.…”

Section: Discussionmentioning

confidence: 68%

Estrogen Treatment Inhibits Vascular Endothelial Senescence and Asymmetrical Dimethylarginine in Ovariectomized Rabbits

Liao

Li²,

Zhou³

et al. 2011

Journal of Cardiovascular Pharmacology

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To investigate the effects of estrogen treatment on aortic endothelial senescence and atherosclerosis, an ovariectomized female rabbit model was constructed, and human umbilical vein endothelial cells were utilized to explore the potential mechanisms. Twenty-eight female rabbits were randomized into 4 groups (7 each): sham operation, ovariectomized, ovariectomized plus low-dose estradiol treatment, and ovariectomized plus high-dose estradiol treatment. All rabbits were fed on high-cholesterol diet for 12 weeks. Blood samples were collected to determine the serum estradiol, asymmetric dimethyl L-arginine (ADMA), and lipid levels, and the aortas were separated for histopathologic analysis. After ovariectomy and high-fat diet, the concentration of serum estradiols declined significantly (P < 0.01) and the levels of ADMA and serum lipids increased (all P < 0.01) as the area of senescent endothelium and atherosclerotic lesions enlarged (both P < 0.01). However, administration of estradiols reduced the levels of ADMA, total cholesterol, and low-density lipoprotein (LDL) cholesterol and inhibited endothelial senescence and atherosclerosis (all P < 0.01). Simultaneously, the concentration of high-density lipoprotein cholesterol and triglyceride increased (all P < 0.01). In vitro experiments also confirmed that estradiols could decrease the ADMA levels induced by oxidized LDL and inhibited oxidized LDL–induced and ADMA-induced human umbilical vein endothelial cell senescence. These results indicate that estrogens can inhibit endothelial senescence and atherosclerosis with reduced ADMA levels and improved lipid profile.

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“…Thus, oral administration of estrogen replacement therapy increased HDL-C and apoA-I levels, decreased total cholesterol and LDL-C and increased triglyceride concentrations in hysterectomized women after 12 weeks [23]. Thus, oral administration of estrogen replacement therapy increased HDL-C and apoA-I levels, decreased total cholesterol and LDL-C and increased triglyceride concentrations in hysterectomized women after 12 weeks [23].…”

Section: Estrogensmentioning

confidence: 97%