Leptin In Postmenopausal Women Research Articles

The effect of Cornus mas fruit extract consumption on lipid profile, glycemic indices, and leptin in postmenopausal women-A randomized clinical trial.

Menopause, which occurs following a declined ovarian activity and reduced estrogen levels, can lead to long-term changes in lipid and glycemic profiles and increases the risk of cardiovascular disease and osteoporosis. Cornelian cherry (Cornus mas) is rich in phytochemicals and antioxidants, which appears to be useful in reducing the postmenopausal complications. This interventional, double-blinded, randomized clinical trial carried out on 84 menopaused women aged 45-60 years old. They were randomly divided into two groups. The treatment group received three capsules of 300 mg of Cornus mas extract (CME), and control group received three capsules of 300 mg of starch powder per day for 8 weeks. Then, BMI, waist circumference, glycemic indices, lipid profile, serum apoproteinase, apoprotein B100, fibrinogen, and leptin were measured. The dietary intakes were evaluated using 24-hr dietary recall questionnaire. The consumption of CME in comparison with the control group resulted in a significant reduction in weight, body mass index, waist circumference, LDL to HDL ratio, total cholesterol to HDL ratio, and fibrinogen. There was also a significant increase in HDL and ApoA1 levels in the treatment group. Furthermore, there was a significant decrease in BMI, waist circumference, fasting insulin, and insulin resistance index after 8 weeks of using CME. Summing up the results, it can be concluded that CME can have possible effects on decreasing BMI, waist circumference, and improving some aspects of lipid profile and glycemic indices in postmenopausal women.

Plasma leptin in postmenopausal women with coronary artery disease: effect of transdermal 17β-estradiol and intermittent medroxyprogesterone acetate

Objectives: In the present study, the relationship between plasma leptin and other cardiovascular risk factors in high-risk postmenopausal women was assessed, as well as the effect of transdermal17β-estradiol unopposed or in combination with intermittent medroxyprogesterone acetate (MPA) on plasma leptin.Methods: Postmenopausal women (n = 118) with coronary artery disease(CAD) were consecutively recruited from women admitted to hospital for coronary angiography. They were randomized to estradiol plus intermittent MPA or to a control group, and investigated at study inclusion,and after 3 and 12 months.Results: A strong relationship was found between leptin and body mass index (r = 0.69, p < 0.001). Leptin was related to lipid fractions (high-densitylipoprotein cholesterol: r = -0.33, p < 0.001; apolipoprotein A: r = -0.28, p = 0.004; and triglycerides: r = 0.27, p = 0.003) and indices of glucosemetabolism (C-peptide: r = 0.47, p < 0.001; fasting insulin: r = 0.42, p < 0.001; glucose: r = 0.25, p = 0.008; insulin resistance: r = 0.45, p< 0.001; and insulin secretion: r = 0.36, p < 0.001). In a multiple regression model, only body mass index (p < 0.001) and C-peptide (p = 0.002) remained as independentfactors for leptin levels. Despite the association with sex hormone-binding globulin (r = 0.30, p = 0.001), no effect on leptin levels was observed with either unopposed transdermal estradiolor estradiol combined with MPA.Conclusion: Plasma leptin is related to other cardiovascular risk factors in postmenopausal women with CAD, but seems to be unaffected by transdermal 17β-estradioladministration.

Acute modifications in the levels of daytime melatonin do not influence leptin in postmenopausal women.

Melatonin shows a clear circadian rhythm with peak values at night, and may act directly with fat cells. Leptin, the anorexic hormone synthesized mainly by adipocytes, is produced in a circadian fashion, similar to that of melatonin. Accordingly, in the present study, we investigated whether melatonin may contribute to the rise in circulating leptin. The study was performed in postmenopausal women with 2 months of treatment with placebo or estradiol (50 microg/day). Melatonin was administered in doses of 1 mg by mouth versus placebo. In experiment 1, melatonin was administered at 08:30 hr. In experiment 2, at 08:30 hr and 10:30 hr, and in experiment 3 at 15:30 hr. Three blood samples, one every 15 min, were collected prior to the administration of melatonin and 2 hr after the administration of the single melatonin dose or the second melatonin administration (experiment 2). Following its administration, circulating melatonin reached pharmacological levels. In the three experiments, levels of leptin were not modified by the daytime administration of melatonin. These data indicate that, at least in daytime hours, acute modifications in daytime melatonin levels do not influence levels of leptin of postmenopausal women either without or with estradiol replacement. Accordingly, the metabolic, endocrine, reproductive and biological modifications induced by acute daytime melatonin in women do not seem to be mediated by modifications in circulating leptin.

Leptin in postmenopausal women: influence of hormone therapy, insulin, and fat distribution.

Whether use of hormone-replacement therapy (HRT) influences menopause-related changes in body weight is unclear. HRT may affect energy balance by influencing synthesis of the adipocyte-derived hormone leptin. The objectives of this study were to: 1) identify factors influencing circulating leptin in postmenopausal women; 2) determine whether HRT influences serum leptin after adjusting for confounding factors; and, 3) identify potential independent effects of HRT or leptin on resting energy expenditure (REE). Subjects were 54 postmenopausal women, 45-55 yr old, 35 of whom used HRT (estrogen plus progestin). Total and regional body composition and fat distribution were determined by dual-energy x-ray absorptiometry and computed tomography; fasting serum leptin and insulin, by RIA; and REE, by indirect calorimetry. Stepwise multiple linear regression analysis indicated that serum leptin could best be predicted from total fat mass, fasting serum insulin, and total lean mass [log leptin = 1.08 x log fat mass) + (0.46 x log insulin) + (-1.25 x log lean mass) + 1.88; model R2 = 0.78, P < 0.001]. Multiple linear regression analysis indicated that visceral fat was independently related to leptin (parameter estimate = 0.23, P < 0.05), after adjusting for s.c. abdominal fat and leg fat, as well as lean mass and insulin. After adjusting for total fat mass, total lean mass, and fasting insulin, serum leptin did not differ between users and nonusers of HRT (21.7 +/- 1.0 vs. 20.2 +/- 1.3 ng/mL, P = 0.369, adjusted mean +/- SE, respectively). Serum estradiol was inversely correlated with (adjusted) leptin in non-HRT users (r = -0.50), suggesting that ovarian senescence may lead to an increase in leptin. Multiple linear regression analysis indicated that REE (adjusted for fat mass, fat-free mass, and ethnicity) was not associated with leptin (P = 0.298) or hormone use status (P = 0.999; 1323 +/- 31 vs. 1316 +/- 42 kcal/day, adjusted mean +/- SE for users and nonusers, respectively). These results indicate that, in postmenopausal women: 1) total fat mass, lean mass, and fasting insulin, but not HRT, are significant determinants of serum leptin; 2) visceral and s.c. fat contribute to serum leptin; and, 3) neither HRT nor leptin is independently related to REE.

Leptin in Postmenopausal Women: Influence of Hormone Therapy, Insulin, and Fat Distribution

Leptin in Postmenopausal Women: Influence of Hormone Therapy, Insulin, and Fat Distribution