Activation of leukocytes by postprandial lipemia in healthy volunteers

Oostrom, A.J.H.H.M. van; Rabelink, Ton J.; Verseyden, C.; Sijmonsma, Tjeerd P.; Plokker, H. W. M.; Jaegere, Peter P.T. de; Cabezas, Manuel Castro

doi:10.1016/j.atherosclerosis.2004.07.004

Cited by 148 publications

(131 citation statements)

References 39 publications

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“…Monocytes from ad-hApoE3 vector-treated mice had reduced surface CD11b, known to be elevated upon monocyte activation in general and following postprandial hyperlipidemia (ref. 41 and Figure 4B). Extending evidence that monocyte activation was reduced, surface CD62L, which is expressed only on the Ly-6C hi monocyte subset (42) and which is shed upon activation, was more abundant on the plasma membrane of Ly-6C hi monocytes after apoE complementation ( Figure 4C).…”

Section: Figurementioning

confidence: 88%

Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe–/– mice during disease regression

Potteaux¹,

Gautier²,

Hutchison³

et al. 2011

J. Clin. Invest.

302

317

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Experimental models of atherosclerosis suggest that recruitment of monocytes into plaques drives the progression of this chronic inflammatory condition. Cholesterol-lowering therapy leads to plaque stabilization or regression in human atherosclerosis, characterized by reduced macrophage content, but the mechanisms that underlie this reduction are incompletely understood. Mice lacking the gene Apoe (Apoe -/-mice) have high levels of cholesterol and spontaneously develop atherosclerotic lesions. Here, we treated Apoe -/-mice with apoEencoding adenoviral vectors that induce plaque regression, and investigated whether macrophage removal from plaques during this regression resulted from quantitative alterations in the ability of monocytes to either enter or exit plaques. Within 2 days after apoE complementation, plasma cholesterol was normalized to wild-type levels, and HDL levels were increased 4-fold. Oil red O staining and quantitative mass spectroscopy revealed that esterified cholesterol content was markedly reduced. Plaque macrophage content decreased gradually and was 72% lower than baseline 4 weeks after apoE complementation. Importantly, this reduction in macrophages did not involve migratory egress from plaques or CCR7, a mediator of leukocyte emigration. Instead, marked suppression of monocyte recruitment coupled with a stable rate of apoptosis accounted for loss of plaque macrophages. These data suggest that therapies to inhibit monocyte recruitment to plaques may constitute a more viable strategy to reduce plaque macrophage burden than attempts to promote migratory egress.

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Section: Figurementioning

confidence: 88%

Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe–/– mice during disease regression

Potteaux¹,

Gautier²,

Hutchison³

et al. 2011

J. Clin. Invest.

302

317

View full text Add to dashboard Cite

show abstract

“…van Oostrom et al (2004) has recently demonstrated that a single meal consisting of fresh cream elicits a mild inflammatory response (van Oostrom et al 2004). Likewise, increases in triglycerides and glucose have been shown to be paralleled by the increased production of proinflammatory cytokines and oxidative stress (Eriksson et al 2001;van Oostrom et al 2003).…”

Section: Discussionmentioning

confidence: 99%

The effects of short-term fish oil supplementation on pulmonary function and airway inflammation following a high-fat meal

2013

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“…Within hours of eating a fatty meal a transient increase in inflammatory markers is seen in the circulation. This reaction appears to be preferentially activated by TAG, SFA and glucose which trigger an acute innate response in circulating monocytes releasing TNFa and IL-6 (69)(70)(71) . The most potent stimulator of the Toll-like receptor 4 (TLR4), the major signalling pathway in the innate immune response, is bacterial LPS or endotoxin.…”

Section: Food and Inflammationmentioning

confidence: 99%

Hypothalamic dysfunction in obesity

Williams

2012

Proc. Nutr. Soc.

115

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A growing number of studies have shown that a diet high in long chain SFA and/or obesity cause profound changes to the energy balance centres of the hypothalamus which results in the loss of central leptin and insulin sensitivity. Insensitivity to these important anorexigenic messengers of nutritional status perpetuates the development of both obesity and peripheral insulin insensitivity. A high-fat diet induces changes in the hypothalamus that include an increase in markers of oxidative stress, inflammation, endoplasmic reticulum (ER) stress, autophagy defect and changes in the rate of apoptosis and neuronal regeneration. In addition, a number of mechanisms have recently come to light that are important in the hypothalamic control of energy balance, which could play a role in perpetuating the effect of a high-fat diet on hypothalamic dysfunction. These include: reactive oxygen species as an important second messenger, lipid metabolism, autophagy and neuronal and synaptic plasticity. The importance of nutritional activation of the Toll-like receptor 4 and the inhibitor of NF-kB kinase subunit b/NK-kB and c-Jun amino-terminal kinase 1 inflammatory pathways in linking a high-fat diet to obesity and insulin insensitivity via the hypothalamus is now widely recognised. All of the hypothalamic changes induced by a high-fat diet appear to be causally linked and inhibitors of inflammation, ER stress and autophagy defect can prevent or reverse the development of obesity pointing to potential drug targets in the prevention of obesity and metabolic dysfunction.Hypothalamus: Obesity: High-fat diet: Inflammation: Neuronal and synaptic plasticityThe developed world is currently facing an epidemic of obesity. Diseases associated with obesity, particularly type 2 diabetes, CVD, cancer, stroke and mental health issues, including dementia (1,2) are provoking a crisis in health care, adversely affecting health and life expectancy and increasing health care costs, estimated to be up to £45 billion by 2050 in the UK alone (3) . Direct and indirect costs of type 2 diabetes, for example, one of the major health consequences of obesity, are currently £21 . 8 billion and set to rise to £35 . 6 billion by 2035-36 in the UK (4) .Obesity is the result of a disproportionately high energy intake compared to energy expenditure and is a complex interaction between environmental and genetic factors (5) with monogenic defects being relatively rare (6) . It seems obvious that an energy-dense diet, high in saturated fat and sugar, should cause weight gain and increased adiposity; nonetheless it appears that these diets cause a profound change in energy balance that does not result from a simple increase in energetic intake. Diet composition, particularly the presence of long-chain saturated fats, results in metabolic dysfunction and increased adiposity and body weight, Abbreviations: AgRP, agouti-related peptide; ARC, arcuate nuclei; CART, cocaine and amphetamine-regulated transcript; CNTF, ciliary neurotrophic factor; ER, endoplasmic reticulum; I...

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Activation of leukocytes by postprandial lipemia in healthy volunteers

Cited by 148 publications

References 39 publications

Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe–/– mice during disease regression

Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of Apoe–/– mice during disease regression

The effects of short-term fish oil supplementation on pulmonary function and airway inflammation following a high-fat meal

Hypothalamic dysfunction in obesity

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