Postprandial inflammation and endothelial dysfuction
Abstract
Postprandial hyperlipidaemia is a common metabolic disturbance in atherosclerosis. During the postprandial phase, chylomicrons and their remnants can penetrate the intact endothelium and cause foam cell formation. These particles are highly atherogenic after modification. People in the Western world are non-fasting for most of the day, which consequently leads to a continuous challenge of the endothelium by atherogenic lipoproteins and their remnants. Furthermore, atherosclerosis is considered a low-grade chronic inflammatory disease. Many studies have shown that the process of atherogenesis in part starts with the interaction between the activated leucocytes and activated endothelium. Postprandial lipoproteins can activate leucocytes in the blood and up-regulate the expression of leucocyte adhesion molecules on the endothelium, facilitating adhesion and migration of inflammatory cells into the subendothelial space. Another inflammatory process associated with postprandial lipaemia is the activation of the complement system. Its central component C3 has been associated with obesity, coronary sclerosis, the metabolic syndrome and fasting and postprandial TAGs (triacylglycerols). Moreover, chylomicrons are the strongest stimulators of adipocyte C3 production via activation of the alternative complement cascade. A postprandial C3 increment has been shown in healthy subjects and in patients with CAD (coronary artery disease) and with FCHL (familial combined hyperlipidaemia). Postprandial lipaemia has been related to TAG and free fatty acid metabolism. All of these mechanisms provide an alternative explanation for the atherogenicity of the postprandial period.
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Other trials did not report improved insulin sensitivity from TNF-a antibody injections despite dampening systemic inflammation.
“In obese non-diabetic or diabetic individuals, several studies have observed improvement of insulin sensitivity after prolonged treatment with neutralising TNF-a antibodies (150,151) , whereas other trials did not report such effects of TNF-a antibody injections, despite dampening of systemic inflammation (152) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [152]
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“Chylomicron remnants as well as fatty acids released dur ing lipoprotein lipasemediated triglyceride hydrolysis are able to induce endothelial activation and dysfunction, expression of cellular adhesion molecules, and activation of monocytes and neutrophils, which can lead to the increase in the recruitment and acti…”
BackgroundPostprandial Lipemia and Subclinical Inflammation on Active Women Taking Oral Contraceptive
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“Moreover, the postprandial inflammatory state (Alipour et al., 2007) triggers microvascular responses such as vasomotor dysfunction, leukocyte recruitment, increased vascular permeability, angiogenesis and thrombosis (Nettleton et al., 2006).”
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“These mechanisms provide an alternative explanation for the atherogenicity of the postprandial period, though there is an association between postprandial lipemia and glycemia.(20,21)”
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“The results from the current study have extended the findings from our previous observations reporting on the association between RA and CV risk factors, by also showing an association with liver fibrosis as estimated by FIB-4 [25, 26, 37].”
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“In the postprandial phase, lipoproteins, including chylomicrons and high-density lipoprotein (HDL), lead to C3 activation in the blood (Alipour et al., 2007).”
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“[25] Alipour A, Elte JW, van Zaanen HC, Rietveld AP, Cabezas MC.”
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BackgroundDisorders in Postprandial Lipid Metabolism and the Risk of Atherogenesis
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“Microarrays were analysed using the reorganized oligonucleotide probes, which combines all individual probes for a gene [8].”
BackgroundMethodInfluential
- Authors
- Alipour, A., Elte, J. W. F., van Zaanen, H. C. T., Rietveld, A. P., & Cabezas, M. C.
- Affiliations
- Sint Franciscus Gasthuis (NL)
- Department of Internal Medicine, St Franciscus Gasthuis, Center for Diabetes and Vascular Medicine, PO Box 10900, 3004 BA Rotterdam, The Netherlands
- Venue
- Biochemical Society Transactions
- Publisher
- Portland Press Ltd.
- Published
- 2007-05-22
- Volume
- 35
- Issue
- 3
- Pages
- 466-469
- ISSN
- 0300-5127 (ISSN-L)
- 1470-8752
- OpenAlex
- W2102556811
- Cited by
- 108
- References
- 47
- Citations by year
- 2025: 4 · 2024: 2 · 2023: 1 · 2021: 3 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 6 · 2016: 7 · 2015: 6 · 2014: 11 · 2013: 6 · 2012: 4
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical Society Transactions (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- endothelial dysfunction, postprandial inflammation, atherosclerosis, chylomicrons, chylomicron remnants, foam cell formation, complement C3, alternative complement pathway, adipocytes, leukocyte activation, coronary artery disease, familial combined hyperlipidaemia, triglycerides, free fatty acids, low-grade inflammation
- MeSH terms
- Animals, Chylomicrons, Complement C3, Endothelium, Vascular, Humans, Hyperlipidemias, Inflammation, Models, Cardiovascular, Postprandial Period, Atherosclerosis
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