scholarly journals Estrogen Deficiency after Menopause Does Not Result in Male Very-Low-Density Lipoprotein Metabolism Phenotype

2010 ◽  
Vol 95 (7) ◽  
pp. 3377-3384 ◽  
Author(s):  
Faidon Magkos ◽  
Elisa Fabbrini ◽  
B. Selma Mohammed ◽  
Bruce W. Patterson ◽  
Samuel Klein ◽  
...  
Keyword(s):  
Postmenopausal Women ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Premenopausal Women ◽  
Reproductive Hormones ◽  
Secretion Rate ◽  
Very Low Density Lipoprotein ◽  
Low Density

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 < 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 < 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.

scholarly journals Association among age, gender, menopausal status and small dense low-density lipoprotein cholesterol: a cross-sectional study

BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e041613
Author(s):  
Toshihide Izumida ◽  
Yosikazu Nakamura ◽  
Yukihiro Sato ◽  
Shizukiyo Ishikawa
Keyword(s):  
Postmenopausal Women ◽  
Low Density Lipoprotein ◽  
Menopausal Status ◽  
Density Lipoprotein ◽  
Premenopausal Women ◽  
Cross Sectional Study ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Cross Sectional

ObjectivesSmall dense low-density lipoprotein cholesterol (sdLDL-C) might be a better cardiovascular disease (CVD) indicator than low-density lipoprotein cholesterol (LDL-C); however, details regarding its epidemiology remain elusive. The present study aimed at evaluating the association between the demographic factors, such as age, gender and menopausal status, and sdLDL-C levels and sdLDL-C/LDL-C ratio in the Japanese population.DesignThis was a cross-sectional study.Setting13 rural districts in Japan, 2010–2017.ParticipantsThis study included 5208 participants (2397 men and 2811 women), who underwent the health mass screening that was conducted in accordance with the medical care system for the elderly and obtained informed consent for this study.ResultsIn total, 517 premenopausal women (mean age ±SD, 45.1±4.2 years), 2294 postmenopausal women (66.5±8.8 years) and 2397 men (64.1±11.2 years) were analysed. In men, the sdLDL-C levels and sdLDL-C/LDL-C ratio increased during younger adulthood, peaked (36.4 mg/dL, 0.35) at 50–54 years, and then decreased. In women, relatively regular increasing trends of sdLDL-C level and sdLDL-C/LDL-C ratio until approximately 65 years (32.7 mg/dL, 0.28), followed by a downward or pleated trend. Given the beta value of age, body mass index, fasting glucose and smoking and drinking status by multiple linear regression analysis, standardised sdLDL-C levels and sdLDL-C/LDL-C ratio in 50-year-old men, premenopausal women and postmenopausal women were 26.6, 22.7 and 27.4 mg/dL and 0.24, 0.15 and 0.23, respectively. The differences between premenopausal and postmenopausal women were significant (p<0.001).ConclusionsSdLDL-C and sdLDL-C/LDL-C ratios showed different distributions by age, gender and menopausal status. A subgroup-specific approach would be necessary to implement sdLDL-C for CVD prevention strategies, fully considering age-related trends, gender differences and menopausal status.

scholarly journals Acute estrogen exposure does not affect basal very low-density lipoprotein–triglyceride production or oxidation in postmenopausal women

2010 ◽  
Vol 163 (3) ◽  
pp. 421-426 ◽  
Author(s):  
Lars C Gormsen ◽  
Christian Høst ◽  
Britta Eilersen Hjerrild ◽  
Claus H Gravholt ◽  
Søren Nielsen
Keyword(s):  
Single Dose ◽  
Postmenopausal Women ◽  
Ex Vivo ◽  
Hormone Replacement ◽  
Low Density Lipoprotein ◽  
Detection Threshold ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Estrogen Exposure

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.

scholarly journals Very Low Density Lipoprotein Metabolism in Patients with Chronic Kidney Disease

2012 ◽  
Vol 2 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Xuewen Wang ◽  
Sharina Belani ◽  
Daniel W. Coyne ◽  
Elisa Fabbrini ◽  
Dominic N. Reeds ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

Effect of simvastatin on plasma lipid and lipoprotein concentrations and low-density lipoprotein metabolism in the nephrotic syndrome

1992 ◽  
Vol 82 (6) ◽  
pp. 701-708 ◽  
Author(s):  
G. L. Warwick ◽  
C. J. Packard ◽  
L. Murray ◽  
D. Grierson ◽  
J. P. Stewart ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Apolipoprotein B ◽  
Cholesterol Synthesis ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Coa Reductase

1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia. 2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways. 3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%). 4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day−1 kg−1). Plasma lathosterol concentration was reduced in all eight patients (range 34–71%), indirectly confirming significant inhibition of cholesterol synthesis. 5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.

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