scholarly journals Dyslipidemia is the hallmark of the metabolic syndrome in postmenopausal women

2020 ◽  
Vol 4 (2) ◽  
pp. 18-21
Author(s):  
Asim Alaaeldin Osman ◽  
Ahmed Mohamed Fadlalla

The incidence of cardiovascular diseases (CVD) increases after menopause and may be due to changes in the plasma lipid-lipoprotein levels that occur following menopausal transition. Physiological estrogen withdrawal during menopause plays a major role in abnormal lipid metabolism such as elevated low-density lipoprotein concentration. The aim of this study was to determine the relationship between dyslipidemia and the causative factors of metabolic syndrome in postmenopausal women. In this cross-sectional study, 290 postmenopausal Sudanese women were included. Lipid profiles were measured by spectrophotometer, estrogen hormone determined by ELISA, insulin resistance determined by HOMA-2 calculator and lipid accumulation product was calculated by the following equation (waist circumference in cm X triglyceride concentration in mM). The results revealed that total cholesterol, triglycerides, low-density lipoprotein levels and very low-density lipoprotein levels were significantly higher in the postmenopausal women with metabolic syndrome (MS) in comparison to those without the MS. Elevated total cholesterol levels were seen in 51.7 %, elevated triglycerides were seen in 49.7% and elevated low-density lipoprotein levels were seen in 29.3% whereas reduced high density lipoprotein levels were seen in 16.89% of the postmenopausal women. Total cholesterol, triglycerides and very low-density lipoprotein values showed a significant positive correlation with insulin resistance and lipid accumulation and a significant negative correlation with the estrogen hormone level. In addition, high density lipoproteins showed a significant negative correlation with lipid accumulation levels.

2010 ◽  
Vol 163 (3) ◽  
pp. 421-426 ◽  
Author(s):  
Lars C Gormsen ◽  
Christian Høst ◽  
Britta Eilersen Hjerrild ◽  
Claus H Gravholt ◽  
Søren Nielsen

ContextLong-term hormone replacement therapy (HRT) with estradiol (E2) is associated with an altered lipid profile including unfavorable increases in triglyceride (TG) concentrations and augmented hepatic very low-density lipoprotein (VLDL)–TG production. There are indications that this effect of estrogens may be immediate.ObjectiveTo study thein vivoeffect of a single dose of E2on VLDL–TG kinetics and oxidation in humans.MethodsEight healthy, postmenopausal women were given a single dose of either placebo or E2(4 mg) orally. VLDL–TG kinetics was assessed by a 240-min primed-continuous infusion ofex vivolabeled [1-14C]triolein-labeled VLDL. Fractional and absolute VLDL–TG oxidation was determined by hyamin trapping of exhaled14C label. Indirect calorimetry provided measurements of lipid oxidation.ResultsAdministration of 4 mg of E2orally rapidly increased plasma E2concentrations from below detection threshold to premenopausal levels. Free fatty acids (FFA) and TG concentrations were unaltered. No immediate effect was observed on either VLDL–TG production (placebo versus E2): 20.0±12.4 vs 24.1±10.7 μmol/min,P=0.33; VLDL–TG oxidation: 12.3±10.9 vs 12.6±5.6 μmol/min,P=0.93); or VLDL–TG clearance rates: 51.4±16.8 vs 64.9±28.8 ml/min,P=0.34).ConclusionsShort-term E2elevation does not affect VLDL–TG production, oxidation, or clearance in humans. We therefore propose that HRT-associated dyslipidemia has a gradual rather than immediate onset.


1990 ◽  
Vol 36 (9) ◽  
pp. 1673-1675 ◽  
Author(s):  
M González Estrada ◽  
C R Rodríguez Ferrer ◽  
I R Astarloa ◽  
E M Lahera

Abstract The values of low-density lipoprotein cholesterol obtained according to the Friedewald formula (Clin Chem 1972; 18:499-502), or by the De Long transformation (J Am Med Assoc 1986;256:2372-7), were compared with the values obtained when the individual cholesterol/triglyceride ratio of very-low-density lipoprotein was used for estimating the contribution of this lipoprotein to the total cholesterol. We found that these formulas gave the greatest errors for individuals with a low serum cholesterol/triglyceride ratio. We propose criteria for deciding when the numerically calculated value of low-density cholesterol is appropriate, and when it is not.


2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Hsiang-Chun Lee ◽  
Shyi-Jang Shin ◽  
Jih-Kai Huang ◽  
Ming-Yen Lin ◽  
Yu-Hsun Lin ◽  
...  

Abstract Background Negatively charged very-low-density lipoprotein (VLDL-χ) in metabolic syndrome (MetS) patients exerts cytotoxic effects on endothelial cells and atrial myocytes. Atrial cardiomyopathy, manifested by atrial remodeling with a dilated diameter, contributes to atrial fibrillation pathogenesis and predicts atrial fibrillation development. The correlation of VLDL-χ with atrial remodeling is unknown. This study investigated the association between VLDL-χ and remodeling of left atrium. Methods Consecutively, 87 MetS and 80 non-MetS individuals between 23 and 74 years old (50.6% men) without overt cardiovascular diseases were included in the prospective cohort study. Blood samples were collected while fasting and postprandially (at 0.5, 1, 2, and 4 h after a unified meal). VLDL was isolated by ultracentrifugation; the percentile concentration of VLDL-χ (%) was determined by ultra-performance liquid chromatography. The correlations of left atrium diameter (LAD) with variables including VLDL-χ, LDL-C, HDL-C, triglycerides, glucose, and blood pressure, were analyzed by multiple linear regression models. A hierarchical linear model was conducted to test the independencies of each variable’s correlation with LAD. Results The mean LAD was 3.4 ± 0.5 cm in non-MetS subjects and 3.9 ± 0.5 cm in MetS patients (P < 0.01). None of the fasting lipid profiles were associated with LAD. VLDL-χ, BMI, waist circumference, hip circumference, and blood pressure were positively correlated with LAD (all P < 0.05) after adjustment for age and sex. Significant interactions between VLDL-χ and blood pressure, waist circumference, and hip circumference were observed. When adjusted for obesity- and blood pressure-related variables, 2-h postprandial VLDL-χ (mean 1.30 ± 0.61%) showed a positive correlation with LAD in MetS patients. Each 1% VLDL-χ increase was estimated to increase LAD by 0.23 cm. Conclusions Postprandial VLDL-χ is associated with atrial remodeling particularly in the MetS group. VLDL-χ is a novel biomarker and may be a therapeutic target for atrial cardiomyopathy in MetS patients. Trial registration ISRCTN 69295295. Retrospectively registered 9 June 2020.


2010 ◽  
Vol 95 (7) ◽  
pp. 3377-3384 ◽  
Author(s):  
Faidon Magkos ◽  
Elisa Fabbrini ◽  
B. Selma Mohammed ◽  
Bruce W. Patterson ◽  
Samuel Klein ◽  
...  

Context: Sex differences in lipid metabolism result in a less proatherogenic plasma lipid profile in premenopausal women than men. The mechanisms responsible for this are unclear but are thought to be related to differences in the sex hormone milieu in men and women. Objective: Our objective was to evaluate the effect of endogenous sex hormones on very-low-density lipoprotein (VLDL) triglyceride (TG) and apolipoprotein B-100 (apoB-100) metabolism. Experimental Design and Main Outcome Measures: We measured basal VLDL-TG and VLDL-apoB-100 concentrations and kinetics by using stable isotope-labeled tracers. Setting and Participants: Eight premenopausal women [age, 43 ± 8 yr; body mass index (BMI), 35 ± 4 kg/m2; mean ± sd], eight postmenopausal women (age, 55 ± 4 yr; BMI, 34 ± 4 kg/m2), and eight men (age, 41 ± 13 yr; BMI, 34 ± 4 kg/m2) were studied at Washington University School of Medicine, St. Louis, MO. Results: VLDL-TG secretion rate was approximately double (P &lt; 0.05) in postmenopausal women and men compared with premenopausal women but not different in postmenopausal women and men. The secretion rate of VLDL-apoB-100 was not different in pre- and postmenopausal women but was greater (P &lt; 0.05) in men than in women. Conclusions: Endogenous ovarian sex steroids are responsible for sexual dimorphism in VLDL-TG secretion, whereas VLDL-apoB-100 secretion is not regulated by female reproductive hormones.


2000 ◽  
Vol 275 (12) ◽  
pp. 8416-8425 ◽  
Author(s):  
Changiz Taghibiglou ◽  
André Carpentier ◽  
Stephen C. Van Iderstine ◽  
Biao Chen ◽  
Debbie Rudy ◽  
...  

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