Postprandial inflammation and endothelial dysfuction

Alipour, Arash; Elte, J.W.F.; Zaanen, H.C.T. van; Rietveld, A.P.; Cabezas, Manuel Castro

doi:10.1042/bst0350466

Cited by 98 publications

(73 citation statements)

References 53 publications

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“…Childhood obesity may place individuals at risk for lifelong metainflammation, since inflammatory markers are elevated in obese children as young as 3 years old (3). Superimposed on this chronic inflammation are recurrent acute episodes of nutrition-related immune activation induced by nutrient availability (fasting or high-fat meals) (4)(5)(6).…”

Section: The Nature Of Obesity-induced Inflammationmentioning

confidence: 99%

Inflammatory links between obesity and metabolic disease

Lumeng¹,

Saltiel²

2011

J. Clin. Invest.

1,969

1,519

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The obesity epidemic has forced us to evaluate the role of inflammation in the health complications of obesity. This has led to a convergence of the fields of immunology and nutrient physiology and the understanding that they are inextricably linked. The reframing of obesity as an inflammatory condition has had a wide impact on our conceptualization of obesity-associated diseases. In this Review, we highlight the cellular and molecular mechanisms at play in the generation of obesity-induced inflammation. We also emphasize how defining the immune regulation in metabolic tissues has broadened the understanding of the diversity of inflammatory responses. IntroductionThe burden of obesity on health extends across multiple organ systems and diseases. While its impact on tissues involved in nutrient regulation is manifest in the development of insulin resistance and type 2 diabetes, there are also unexpected connections between obesity and the risk of cancer and pulmonary diseases. Over the past decade, the search for a potential unifying mechanism behind the pathogenesis of obesity-associated diseases has revealed a close relationship between nutrient excess and derangements in the cellular and molecular mediators of immunity and inflammation. This has given birth to the concept of "metainflammation" (1) to describe the chronic low-grade inflammatory response to obesity. We present here a broad overview of the links between obesity and immune responses with a focus on metabolic disease and argue that the intersection between the pathways that control nutrient metabolism and inflammatory responses may be broadly applicable to our understanding of inflammation and the immune system.

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Section: The Nature Of Obesity-induced Inflammationmentioning

confidence: 99%

Inflammatory links between obesity and metabolic disease

Lumeng¹,

Saltiel²

2011

J. Clin. Invest.

1,969

1,519

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“…A high-fat diet increases the risk for acute and chronic inflammation (1,2) and for chronic inflammatory diseases such as atherosclerosis and diabetes (3)(4)(5). The proinflammatory effect of fatty diets has mainly been attributed to the inflammatory properties of dietary fatty acids.…”

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confidence: 99%

“…Once in the systemic circulation, these large lipoprotein particles can release significant amounts of free fatty acids upon interaction with lipoprotein lipases tethered to the endothelium, and this might partially explain the putative proinflammatory and proatherogenic potential of these lipoproteins (1,13,14). However, chylomicrons also have high affinity for LPS (15)(16)(17) and thus not only transport postprandial fat, but likely also significant amounts of concomitantly absorbed gut LPS.…”

mentioning

confidence: 99%

Chylomicrons promote intestinal absorption of lipopolysaccharides

Ghoshal

Witta

Zhong

et al. 2009

Journal of Lipid Research

554

387

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Recent data suggest that dietary fat promotes intestinal absorption of lipopolysaccharides (LPS) from the gut microflora, which might contribute to various inflammatory disorders. The mechanism of fat-induced LPS absorption is unclear, however. Intestinal-epithelial cells can internalize LPS from the apical surface and transport LPS to the Golgi. The Golgi complex also contains newly formed chylomicrons, the lipoproteins that transport dietary longchain fat through mesenteric lymph and blood. Because LPS has affinity for chylomicrons, we hypothesized that chylomicron formation promotes LPS absorption. In agreement with our hypothesis, we found that CaCo-2 cells released more cell-associated LPS after incubation with oleic-acid (OA), a long-chain fatty acid that induces chylomicron formation, than with butyric acid (BA), a short-chain fatty acid that does not induce chylomicron formation. Moreover, the effect of OA was blocked by the inhibitor of chylomicron formation, Pluronic L-81. We also observed that intragastric triolein (TO) gavage was followed by increased plasma LPS, whereas gavage with tributyrin (TB), or TO plus Pluronic L-81, was not. Most intestinally absorbed LPS was present on chylomicron remnants (CM-R) in the blood. Chylomicron formation also promoted transport of LPS through mesenteric lymph nodes (MLN) and the production of TNFa mRNA in the MLN. Together, our data suggest that intestinal epithelial cells may release LPS on chylomicrons from cell-associated pools. Chylomicron-associated LPS may contribute to postprandial inflammatory responses or chronic diet-induced inflammation in chylomicron target tissues.-Ghoshal, S., J. Witta, J. Zhong, W. de Villiers, and E. Eckhardt. Chylomicrons promote intestinal absorption of lipopolysaccharides. J. Lipid Res. 2009. 50: 90-97.

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“…The most adequate way to experimentally reproduce the postprandial lipemia condition appears to be the administration of a standardized OFL to fasting patients. 28 This model has been widely applied in relatively small sample of subjects to study the postprandial lipemia effect on inflammatory parameters, 29,30 circulating markers of endothelial dysfunction 31,32 and prothrombotic variables. 33,34 So, we observed that 6-month treatment is associated to a significant improvement of basal level of sICAM-1 (À17.3%), IL-6 (À31.6%) and Hs-CRP (À33.3%) in nondiabetics, whereas in BG (À3.7%), Tg (À11.2%), sICAM-1 (À16.5%), IL-6 (À36.6%) and Hs-CRP (À25.0%) in diabetics.…”

Section: Discussionmentioning

confidence: 99%

Candesartan effect on inflammation in hypertension

et al. 2010

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The aim of this study was to evaluate the effect of candesartan on inflammatory biomarkers in hypertensive patients with and without type 2 diabetes mellitus after a standardized oral fat load (OFL). A total of 219 patients were enrolled: 106 patients were assigned to the non-diabetic hypertensive (NH) group, and 113 to the diabetic hypertensive (DH) group. All patients received candesartan therapy for 6 months and underwent a standardized OFL at baseline and after 6 months of therapy. We evaluated systolic blood pressure (SBP) and diastolic blood pressure (DBP), blood glucose (BG), triglycerides (Tg), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and high-sensitivity C reactive protein (Hs-CRP). At baseline, glycated hemoglobin, homeostasis model assessment insulin resistance index, BG, fasting plasma insulin, Tg, sICAM-1, IL-6 and Hs-CRP in the DH group were significantly higher, whereas high-density lipoprotein-cholesterol value was significantly lower compared to NH group. After 6 months of candesartan therapy, sICAM-1, IL-6 and Hs-CRP were significantly lower compared to baseline in both groups; furthermore, there was a significant decrease of SBP and DBP values in both groups. After the OFL administered at baseline, there was an increase of Tg, sICAM-1, IL-6 and Hs-CRP in both groups. After the OFL administered after 6 months of therapy, instead, there was no significant variation of BG, Tg or sICAM-1 value in both groups, whereas there was an increase of IL-6 and Hs-CRP compared to time 0. We observed that candesartan treatment attenuated the inflammatory answer in both groups of patients, even if more efficiently in nondiabetic ones.

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Postprandial inflammation and endothelial dysfuction

Cited by 98 publications

References 53 publications

Inflammatory links between obesity and metabolic disease

Inflammatory links between obesity and metabolic disease

Chylomicrons promote intestinal absorption of lipopolysaccharides

Candesartan effect on inflammation in hypertension

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