The induction of macrophage foam cell formation by chylomicron remnants

Botham, Kathleen M.; Moore, Elizabeth Hernández; Pascale, C. De; Bejta, Fatos

doi:10.1042/bst0350454

Cited by 57 publications

(46 citation statements)

References 39 publications

(58 reference statements)

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“…Meanwhile, ATP attenuated fat deposition in cardiac epicardium and reduced foam cells in thoracic aorta. It is well known that foam cell promotes the formation of fatty streak in blood vessels that is an early marker of atherosclerosis (Botham et al 2007;Yu et al 2013). It is generally accepted that total TG levels are an independent predictor for coronary heart diseases (Imke et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Zhang

Liang

Tong

et al. 2016

Pharmaceutical Biology

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Context Recently, adenosine triphosphate (ATP) was occasionally found to decrease the triglyceride (TG) levels in several hyperlipidemic patients in our clinical practice. Objective The study investigates the anti-hyperlipidemic effects of ATP in a high-fat fed rabbit model and hyperlipidemic patients. Materials and methods Twenty-four rabbits were randomly divided into three groups of eight animals each as follows: normal diet, high-fat diet and high-fat diet + ATP group. ATP supplementation (40 mg/day) was started at the 20th day and lasted for 10 days. Serum concentrations of total cholesterol (TC), TG, LDL-C, HDL-C were measured on the 20th day and 30th day. Heart, liver and aorta were subjected histopathological examination. Twenty outpatients diagnosed primary hyperlipidemia took ATP at a dose of 60 mg twice a day for 1 week.Results Feeding rabbits with a high-fat diet resulted in a significant elevation of lipid parameters including TC, TG, LDL-C, VLDL-C compared to the normal diet group (p50.01). ATP treatment significantly decreased serum TG level (p50.01), whilst other parameters remained statistically unaltered. Meanwhile, ATP significantly reduced the thickness of fat layer in cardiac epicardium (p50.05) and pathological gradation of ballooning degeneration in hepatocytes (p50.05). After taking ATP for 1 week, hyperlipidemia patients exhibited a significant decrease of TG (p50.01), but other lipid parameters had no significant change. Discussion and conclusion The study indicates that ATP selectively decreases serum TG levels in high-fat diet rabbits and hyperlipidemic patients. Therefore, ATP supplementation may provide an effective approach to control TG level. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Zhang

Liang

Tong

et al. 2016

Pharmaceutical Biology

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“…The uptake of matrix-retained lipoproteins by macrophages and smooth muscle cells leads to the formation of foam cells storing a large amount of CE. 50,70,73) However, native LDL is incapable of generating foam cells from macrophages. 74) The uptake of modified lipoproteins by macrophages is a complex process involving receptor-mediated endocytosis and phagocytosis.…”

Section: Foam Cell Formationmentioning

confidence: 99%

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

133

108

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Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies.

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“…CMR have been shown to penetrate the artery wall and to be retained within the intima [28][29][30], and remnant-like lipoproteins have been found in human atherosclerotic plaque [31][32][33]. CMR and TRLs have also been demonstrated to cause endothelial dysfunction [34][35][36][37][38], macrophage foam cell formation [34,39] and the proliferation of VSMCs [34]. Other pro-inflammatory and potentially atherogenic effects of postprandial lipoproteins include activation of leukocytes, promoting adhesion to the endothelium and invasion of the artery wall [12,40].…”

Section: Postprandial Hyperlipidemia As a Risk Factor For Atherosclermentioning

confidence: 99%

“…Atherosclerosis is the main cause of the increased morbidity and mortality seen in obese patients and is a major cause of death in diabetic patients, and disturbances in postprandial lipid metabolism are particularly implicated in the increased risk [39]. Insulin resistance, a condition commonly found across the different metabolic diseases, is believed to be the primary contributory factor to the postprandial hyperlipidemia [83].…”

Section: Postprandial Lipemia and Metabolic Dis-easesmentioning

confidence: 99%

“…In addition, it has been suggested that alterations in the production or action of glucagon-like peptide-1 and -2, which have been implicated in the regulation of CM formation, may also play a role [84]. The delayed clearance of the intestinally derived lipoproteins is believed to be caused by a reduction in the activity of LPL and hepatic lipase, increased competition for lipolysis by LPL because of the rise in VLDL levels, and decreased uptake by the liver due to lower concentrations of apoE in the particles, increased competition for receptors from VLDL and impairment by hyperglycemia [39,81,83,87].…”

Section: Postprandial Lipemia and Metabolic Dis-easesmentioning

confidence: 99%

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Postprandial Lipid Metabolism: The Missing Link Between Life-Style Habits and the Increasing Incidence of Metabolic Diseases in Western Countries?~!2009-09-30~!2010-01-26~!2010-03-30~!

Bravo¹,

Napolitano²,

Botham³

2010

TOTRANSMJ

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Postprandial lipemia is the transient increase in blood lipids which occurs after a meal containing fat and is caused by raised levels of triglyceride-rich lipoproteins (TRLs) in the blood. Delayed clearance of TRLs leads to postprandial hyperlipidemia, and there is now a great deal of evidence to support the idea that this condition is an important risk factor for cardiovascular disease (CVD). Western lifestyle habits including: diets low in fresh fruit and vegetables and high in fat and processed food, alcohol consumption, smoking, and lack of exercise tend to promote postprandial hyperlipidemia, and it is a characteristic feature of increasingly common metabolic diseases such as obesity, insulin resistance and type 2 diabetes which are also linked to modern lifestyle behaviour and which carry an increased risk of CVD development. Modification of lifestyle factors such as changing to a healthier diet, weight loss, reducing alcohol consumption and increasing exercise can cause significant reductions in postprandial hyperlipidemia and thus help to reduce this risk. Despite the growing recognition that the extent of postprandial lipemia is a good predictor of CVD, no standardized methodology for its measurement is currently available. Determination of blood TG levels after consumption of a standard test meal is likely to be the most convenient approach for a routine clinical test, and we propose a standard test meal which is easily adaptable for the variations in dietary habits in different countries. Greater use of postprandial lipid determination will aid in the translation of our extensive knowledge on the role of nutrition in health into national and international policy.

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The induction of macrophage foam cell formation by chylomicron remnants

Cited by 57 publications

References 39 publications

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Postprandial Lipid Metabolism: The Missing Link Between Life-Style Habits and the Increasing Incidence of Metabolic Diseases in Western Countries?~!2009-09-30~!2010-01-26~!2010-03-30~!

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