Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. Remnant lipoproteins become attached to the vascular wall, where they can penetrate intact endothelium causing foam cell formation. Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate the expression of endothelial adhesion molecules, facilitate adhesion and migration of inflammatory cells into the subendothelial space, and activate the complement system. Since humans are postprandial most of the day, the continuous generation of remnants after each meal may be one of the triggers for the development of atherosclerosis. Modulation of postprandial lipemia by lifestyle changes and pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options.
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http://dx.doi.org/10.1155/2012/947417 | DOI Listing |
Exp Physiol
January 2025
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK.
In health, the liver is a metabolically flexible organ that plays a key role in regulating systemic lipid and glucose concentrations. There is a constant flux of fatty acids (FAs) to the liver from multiple sources, including adipose tissue, dietary, endogenously synthesized from non-lipid precursors, intrahepatic lipid droplets and recycling of triglyceride-rich remnants. Within the liver, FAs are used for triglyceride synthesis, which can be oxidized, stored or secreted in very low-density lipoproteins into the systemic circulation.
View Article and Find Full Text PDFNutrients
January 2025
Faculty of Agriculture and Food Technology, Latvia University of Life Sciences and Technologies, LV-3001 Jelgava, Latvia.
Hormonal changes throughout a woman's life cycle significantly affect serum lipid levels. Alterations in the serum lipid profile can increase the risk of cardiovascular diseases (CVDs). Additionally, nutrition and dietary habits are crucial for managing dyslipidemia.
View Article and Find Full Text PDFBiomedicines
December 2024
Guangdong Provincial Key Laboratory of Tropical Disease Research, Department of Radiation Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, China.
The relationship between lipid profiles, telomere length (TL), and cancer risk remains unclear. This study employed two-sample Mendelian randomization (MR) with mediation analysis to investigate their causal relationships, examining lipid profiles as exposure, TL as mediator, and nine cancer types as outcomes. We conducted our analysis using two-stage least squares (2SLS) regression integrated with inverse variance weighted (IVW) methods to address potential endogeneity and strengthen our causal inference.
View Article and Find Full Text PDFLipids Health Dis
January 2025
Department of Medical Biosciences, Clinical Chemistry, Umeå University, Building 6M 2:Nd Floor, 901 85, Umeå, Sweden.
Background: The ABO blood group system has shown an association with cardiovascular disease. The susceptibility to CVD is proposed to be partly mediated by dyslipidaemia in non-O individuals. Previous studies are scarce for the RhD blood group, but we recently showed that RhD - young individuals are associated with subclinical atherosclerosis.
View Article and Find Full Text PDFBMC Med
January 2025
Health and Social Research Center, Universidad de Castilla-La Mancha, Cuenca, Spain.
Background: Recent evidence from both randomized controlled trials and cohort studies in adults suggests that plasma remnant cholesterol (RC) levels predict cardiovascular disease. In children, studies are scarce, although high levels of RC might represent a marker of early atherosclerotic damage. Thus, the aim of this study was to explore the cardiometabolic risk associated with RC, which extends beyond low-density lipoprotein cholesterol (LDL-c) in children.
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