Increased activity of lecithin: Cholesterol acyltransferase during short-term oral estrogen progestin replacement therapy in a group of postmenopausal women

A metabolomics study of the inhibitory effect of 17-beta-estradiol on osteoclast proliferation and differentiation

“…These results were consistent with the previous reports that oral administration of estradiol could increase the activity of LCAT in the blood. [64][65][66] LysoPCs can be decomposed by the high expression of LCAT to compose cholesterol ester, 53 which may partly account for the decreased level of LysoPCs along with decreased oxidative stress. Additionally, LCAT could convert phosphatidylcholines (PCs) to lysophosphatidylcholines (LysoPCs), and through which modulate the levels of PCs and LysoPCs.…”

17β-Estradiol and ICI-182780 regulate the hair follicle cycle in mice through an estrogen receptor-α pathway

“…However, E 2 is also produced at many nonovarian sites (adipose tissues, testes, various brain regions, and adrenals) (42) and can exert profound effects in nonreproductive organs in both females and males. For example, E 2 was found to modify arterial smooth muscle response (1,22), bone formation and growth (39,43), brain function (3,4), and levels of low-and high-density lipoproteins (24,37). More recently, E 2 has also been demonstrated to be involved in the regulation of the hair follicle cycle in mice (29).…”

Lipoproteins and low‐dose estradiol replacement therapy in post‐menopausal Type 2 diabetic patients: the effect of addition of norethisterone acetate

“…Ulloa et al . [39] have demonstrated in non‐diabetic subjects an increase in LCAT following treatment with conjugated equine oestrogen/medroxyprogestin acetate therapy. This study together with the present results adds further support to a role of oestrogen/progestogen in the increase in cellular cholesterol mobilization.…”