Effects of oestradiol and levonorgestrel on lipoprotein lipids and postheparin plasma lipase activities in normolipoproteinaemic women

Abstract

The effects of oestradiol and levonorgestrel on plasma lipoprotein cholesterol (Chol) and triglyceride (Tg) levels and on postheparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activity were studied in 52 normolipoproteinaemic women. The androgen-derived progestin levonorgestrel increased postheparin plasma hepatic lipase (PH-HL) activity and decreased plasma high-density lipoprotein (HDL) lipid concentrations in a manner opposite to that of oestradiol. The relationships between PH-HL activity and HDL lipids suggest an important role for this enzyme as a mediator of sex hormone action on HDL.The sex differences in the distribution of plasma lipoproteins were demonstrated nearly three de¬ cades ago by Russ et al. ( 1951). Young women were shown to have a relatively greater amount of alpha lipoprotein (HDL) and a correspondingly smaller amount of beta lipoprotein (LDL) than young men. This stimulated the interest in the effects of sex hormones on plasma lipoproteins. Oestrogens were shown to increase alpha lipoprotein and decrease beta lipoprotein concentrations whereas androgens had the opposite effect (Russ et al. 1955). Also, oestrogens increased plasma very-low density lipo¬ protein (VLDL) concentrations whereas androgens reduced them (Furman et al. 1967). Later on nortestosterone-derived progestins were shown to have androgen-like effects on plasma lipoprotein levels (Silfverstolpe et al. 1979; Hirvonen et al. 1981), whereas progesterone and its dérivâtes were relatively inert in this respect (Svanborg & Vikrot 1966; Silfverstolpe et al. 1979; Hirvonen et al. 1981).The mechanism by which sex hormones exert their effects on plasma lipoprotein levels is not clear. Interestingly, they also influence postheparin plasma hepatic lipase (PH-HL) activity. Equine oestrogens have a marked suppressing effect on PH-HL activity whereas postheparin plasma lipo¬ protein lipase (PH-LPL) activity is not affected (Applebaum et al. 1977). A similar effect was observed during treatment with oestradiol valerate in hypercholesterolaemic post-menopausal women (Tikkanen et al. 1979). Conversely, the synthetic nortestosterone-derived progestin levonorgestrel is known to increase PH-HL activity (Tikkanen et al. 1981). In the present study we treated normo¬ lipoproteinaemic women with oestradiol and levo¬ norgestrel in order to clarify the possible role of hepatic lipase as mediator of sex hormone effects on lipoprotein lipids. Material and MethodsThree groups of women received hormone therapy. In Group 1 women were given oestradiol only, in Group 2 they received levonorgestrel only and in Group 3 a combination of both was given. The women in all three groups had normal plasma lipoprotein levels prior to hormone treatment. The mean pre-treatment concentra¬ tions are given in Table 1. Apart from symptoms related Third Department ofMedicine1,

Hepatic lipase and dyslipidemia: interactions among genetic variants, obesity, gender, and diet

“…Estrogen replacement therapy in postmenopausal women acutely reduces HL activity (18,19,66). Colvin et al demonstrated that orally administered micronized estradiol suppressed HL activity and increased HDL in a dose-dependent manner (64,67).…”

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

“…In man, some studies have failed to demonstrate effects of oral estrogen on either adipose tissue (22) or postheparin plasma LPL (22)(23)(24)(25), while others have reported that oral estrogen inhibits postheparin plasma LPL in postmenopausal women (26,27). Oral or percutaneous progestin alone (24,28,29), or in combination with estrogen (30), may enhance LPL activity in adipose tissue (28, 29) and postheparin plasma (24), respectively, while no effect on postheparin plasma LPL has been observed with low dose oral contraceptive (31) and anabolic steroid (31,32).…”

Tratamento pós-menopausa reduz a atividade da catalase e atenua o risco cardiovascular

“…In contrast, it has been reported that while HT may prevent the development of atherosclerotic plaques in postmenopausal women 9 , there is no difference in the carotid IMT between women who had and had not used HT 11 . Lipid and lipoprotein metabolism is markedly altered after menopause [12][13][14] with a natural reduction in estrogen levels.…”

“…The presence of menopause was defined among women ≥ 40 years old with at least one year of natural menopause or surgical bilateral oophorectomy, in accordance with the criteria of the North American Menopause Society 14 . The exclusion criteria for participation in the study were: severe dyslipidemia (HDL cholesterol ≤ 40 mg/L, LDL cholesterol ≥ 190 mg/L and triglycerides ≥ 400 mg/L), smoking, alcoholism, severe systemic disease including nephropathy, endocrinopathy and pneumopathy.…”

“…Vasomotor symptoms (hot flashes and night sweats) were the main indication for the use of systemic HT 14 . All POMW had been on HT with continuous oral estrogen (0.625 mg/d) or continuous estrogen (0.625 mg/d) and methoxyprogesterone acetate (2.5 or 5 mg/d) for at least one year (mean of five years).…”