Habitual consumption of eggs does not alter the beneficial effects of endurance training on plasma lipids and lipoprotein metabolism in untrained men and women

2009 ◽  
Vol 20 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Lisa M. Vislocky ◽  
Matthew A. Pikosky ◽  
Kristin Herron Rubin ◽  
Sonia Vega-López ◽  
P. Courtney Gaine ◽  
...  
Keyword(s):  
Endurance Training ◽  
Plasma Lipids ◽  
Lipoprotein Metabolism ◽  
Men And Women ◽  
Beneficial Effects

scholarly journals Sex Differences in Lipid and Lipoprotein Metabolism: It's Not Just about Sex Hormones

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1192-1192
Author(s):  
Xuewen Wang ◽  
Faidon Magkos ◽  
Bettina Mittendorfer
Keyword(s):  
Sex Differences ◽  
Sex Hormones ◽  
Plasma Lipids ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Men And Women ◽  
Beneficial Effects ◽  
Physiological Alterations ◽  
First Pass ◽  
Hormonal Milieu

Abstract It is commonly thought that sex hormones are important regulators of plasma lipid kinetics and are responsible for sexual dimorphism in the plasma lipid profile. Here we discuss the findings from studies evaluating lipid and lipoprotein kinetics in men and women in the context of what we know about the effects of exogenous sex hormone administration, and we conclude that it is more complicated than that. It has become clear that normal physiological alterations in the hormonal milieu (i.e. due to menopause or throughout the menstrual cycle) do not significantly affect plasma lipid homeostasis. Furthermore, parenterally administered estrogens have either no effect or only very small beneficial effects, whereas orally administered estrogens raise plasma triglyceride concentrations—a phenomenon that is not consistent with the observed sex differences and likely results from the hepatic “first-pass effect.” The effects of progestogens and androgens mimic only in part the differences in plasma lipids between men and women. Thus, the underlying physiological modulators of plasma lipid metabolism responsible for the differences between men and women remain to be elucidated.

scholarly journals Sex Differences in Lipid and Lipoprotein Metabolism: It's Not Just about Sex Hormones

2011 ◽  
Vol 96 (4) ◽  
pp. 885-893 ◽  
Author(s):  
Xuewen Wang ◽  
Faidon Magkos ◽  
Bettina Mittendorfer
Keyword(s):  
Sex Differences ◽  
Sex Hormones ◽  
Plasma Lipids ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Men And Women ◽  
Beneficial Effects ◽  
Physiological Alterations ◽  
First Pass ◽  
Hormonal Milieu

Abstract It is commonly thought that sex hormones are important regulators of plasma lipid kinetics and are responsible for sexual dimorphism in the plasma lipid profile. Here we discuss the findings from studies evaluating lipid and lipoprotein kinetics in men and women in the context of what we know about the effects of exogenous sex hormone administration, and we conclude that it is more complicated than that. It has become clear that normal physiological alterations in the hormonal milieu (i.e. due to menopause or throughout the menstrual cycle) do not significantly affect plasma lipid homeostasis. Furthermore, parenterally administered estrogens have either no effect or only very small beneficial effects, whereas orally administered estrogens raise plasma triglyceride concentrations—a phenomenon that is not consistent with the observed sex differences and likely results from the hepatic “first-pass effect.” The effects of progestogens and androgens mimic only in part the differences in plasma lipids between men and women. Thus, the underlying physiological modulators of plasma lipid metabolism responsible for the differences between men and women remain to be elucidated.

Plasma Lipids, Lipoprotein Metabolism and HDL Lipid Transfers are Equally Altered in Metabolic Syndrome and in Type 2 Diabetes

Lipids ◽  
2014 ◽  
Vol 49 (7) ◽  
pp. 677-684 ◽  
Author(s):  
Vanessa M. Silva ◽  
Carmen G. C. Vinagre ◽  
Luis A. O. Dallan ◽  
Ana P. M. Chacra ◽  
Raul C. Maranhão
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Plasma Lipids ◽  
Lipoprotein Metabolism

Endurance training in older men and women II. Blood lactate response to submaximal exercise

1984 ◽  
Vol 57 (4) ◽  
pp. 1030-1033 ◽  
Author(s):  
D. R. Seals ◽  
B. F. Hurley ◽  
J. Schultz ◽  
J. M. Hagberg
Keyword(s):  
Endurance Training ◽  
Blood Lactate ◽  
Respiratory Exchange Ratio ◽  
Submaximal Exercise ◽  
Older Individuals ◽  
O2 Uptake ◽  
Men And Women ◽  
Low Intensity ◽  
Older Men And Women ◽  
Intensity Training

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61–67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65–90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.

scholarly journals Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Dietary Fats ◽  
Low Density ◽  
Mrna Levels ◽  
Expression Of Genes ◽  
Coa Reductase

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.

Abstract 69: Anacetrapib Dose-dependently Decreases Atherosclerosis Development and Adds to the Beneficial Effects of Atorvastatin in APOE*3Leiden.CETP Mice

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Susan Kühnast ◽  
Sam J van der Tuin ◽  
Louis M Havekes ◽  
Ko Willems van Dijk ◽  
Patrick C Rensen ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Plasma Lipids ◽  
Atherosclerotic Lesion ◽  
Hdl Cholesterol ◽  
Statin Treatment ◽  
Epidemiological Studies ◽  
Lesion Size ◽  
Beneficial Effects ◽  
Atherosclerosis Development ◽  
C 32

Introduction The residual risk of cardiovascular disease that remains after statin treatment has triggered the search for a secondary treatment target. Epidemiological studies propose HDL-cholesterol (HDL-C) as a possible candidate. Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from atheroprotective HDL to atherogenic (V)LDL. In human intervention trials, the CETP inhibitor anacetrapib decreases (V)LDL-C by 30-40% and increases HDL-C by 40-140%. Hypothesis Complete inhibition of CETP activity may result in adverse effects as compared to partial inhibition due to the appearance of a dysfunctional HDL. We, therefore, evaluated the effect of a broad treatment window of anacetrapib-induced CETP inhibition with partial to full inhibition, as well as the combination of atorvastatin and anacetrapib on atherosclerosis development in APOE*3Leiden.CETP mice. Methods Female mice were fed a Western-type diet containing 0.1% cholesterol without or with incremental dosages of anacetrapib (0.03; 0.3; 3; 30 mg/kg/d), atorvastatin (2.4 mg/kg/d) or a combination of anacetrapib (0.3 mg/kg/d) and atorvastatin (2.4 mg/kg/d) for 20 weeks. Effects on plasma lipids, CETP activity and levels, as well as atherosclerotic lesion size and severity were assessed. Results Anacetrapib dose-dependently reduced CETP activity (-60% to -100%, P<0.001) and increased CETP levels (+13% to +31%, P<0.05), thereby decreasing nonHDL-C (-23% to -44%, P<0.001) and increasing HDL-C (+32% to +88%, P<0.001). Atorvastatin decreased CETP activity (-29%, P<0.001) and nonHDL-C (-36%, P<0.001). Anacetrapib dose-dependently decreased atherosclerotic lesion size (-36%, P<0.05 to -92%, P<0.001) and the percentage severe lesions. Anacetrapib added to the effects of atorvastatin by further reducing nonHDL-C (-36%, P<0.001), increasing HDL-C (+72%, P<0.001) and decreasing lesion size (-86%, P<0.001) and severity. Results on lesion composition are pending. Conclusions Anacetrapib dose-dependently decreases atherosclerosis development and adds to the beneficial effects of atorvastatin in APOE*3Leiden.CETP mice. Total blockage of CETP activity does not reveal adverse effects as compared to partial blockage.

Longitudinal study of dietary intakes and plasma lipids in healthy elderly men and women

1992 ◽  
Vol 55 (3) ◽  
pp. 682-688 ◽  
Author(s):  
P J Garry ◽  
W C Hunt ◽  
K M Koehler ◽  
D J VanderJagt ◽  
B J Vellas
Keyword(s):  
Longitudinal Study ◽  
Plasma Lipids ◽  
Dietary Intakes ◽  
Elderly Men ◽  
Men And Women ◽  
Healthy Elderly

Smartphone interactions and mental well-being in young adults: A longitudinal study based on objective high-resolution smartphone data

2020 ◽  
pp. 140349482092041
Author(s):  
Agnete Skovlund Dissing ◽  
Naja Hulvej Rod ◽  
Thomas A. Gerds ◽  
Rikke Lund
Keyword(s):  
Young Adults ◽  
Depressive Symptoms ◽  
Well Being ◽  
Large Network ◽  
Men And Women ◽  
Beneficial Effects ◽  
Disturbed Sleep ◽  
Mental Well Being ◽  
Over Time

Aims: To investigate the effects of objectively measured smartphone interactions on indicators of mental well-being among men and women in a population of young adults. Methods: A total of 816 young adults (mean±SD age 21.6±2.6 years; 77% men) from the Copenhagen Network Study were followed with objective recordings of smartphone interactions from calls, texts and social media. Participants self-reported on loneliness, depressive symptoms and disturbed sleep at baseline and in a four-month (interquartile range 75–163 days) follow-up survey. Multiple linear regression was used to analyse the association between smartphone interactions and mental well-being separately for men and women. Results: A higher number of smartphone interactions was associated with lower levels of loneliness at baseline and the same pattern appeared for depressive symptoms, although this was less pronounced. A high level of smartphone interaction was associated with lower levels of disturbed sleep for men, but not for women. In follow-up analyses, a high versus low level of smartphone interaction was associated with an increase in loneliness and depressive symptoms over time for women, but not for men. Conclusions: Smartphone interactions are related to better mental well-being, which may be attributed to the beneficial effects of an underlying social network. Over time, accommodating a large network via smartphone communication might, however, have negative effects on mental well-being for women.

scholarly journals ILRUN , a Human Plasma Lipid GWAS Locus, Regulates Lipoprotein Metabolism in Mice

2020 ◽  
Vol 127 (11) ◽  
pp. 1347-1361 ◽  
Author(s):  
Xin Bi ◽  
Takashi Kuwano ◽  
Paul C. Lee ◽  
John S. Millar ◽  
Li Li ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Peroxisome Proliferator ◽  
Nucleotide Polymorphisms ◽  
Genetic Associations ◽  
Peroxisome Proliferator Activated Receptor ◽  
Liver Transcriptome ◽  
Artery Disease

Rationale: Single-nucleotide polymorphisms near the ILRUN (inflammation and lipid regulator with ubiquitin-associated–like and NBR1 [next to BRCA1 gene 1 protein]-like domains) gene are genome-wide significantly associated with plasma lipid traits and coronary artery disease (CAD), but the biological basis of this association is unknown. Objective: To investigate the role of ILRUN in plasma lipid and lipoprotein metabolism. Methods and Results: ILRUN encodes a protein that contains a ubiquitin-associated–like domain, suggesting that it may interact with ubiquitinylated proteins. We generated mice globally deficient for Ilrun and found they had significantly lower plasma cholesterol levels resulting from reduced liver lipoprotein production. Liver transcriptome analysis uncovered altered transcription of genes downstream of lipid-related transcription factors, particularly PPARα (peroxisome proliferator-activated receptor alpha), and livers from Ilrun -deficient mice had increased PPARα protein. Human ILRUN was shown to bind to ubiquitinylated proteins including PPARα, and the ubiquitin-associated–like domain of ILRUN was found to be required for its interaction with PPARα. Conclusions: These findings establish ILRUN as a novel regulator of lipid metabolism that promotes hepatic lipoprotein production. Our results also provide functional evidence that ILRUN may be the casual gene underlying the observed genetic associations with plasma lipids at 6p21 in human.

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