The impact of dietary fatty acids on macrophage cholesterol homeostasis

Afonso, Milessa da Silva; Castilho, Gabriela; Lavrador, Maria Sílvia Ferrari; Passarelli, Marisa; Nakandakare, Edna Regina; Lottenberg, Simão Augusto; Lottenberg, Ana Maria

doi:10.1016/j.jnutbio.2013.10.001

Cited by 30 publications

(21 citation statements)

References 78 publications

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“…Atherosclerosis, the major cause of CVD, is considerably affected by dietary fat consumption . Conflicting reports regarding the role of SO and particularly that of LA in CVD and atherogenesis , have led us to focus on their effects on oxidative stress and lipid metabolism in macrophages, the predominant cells in early atherogenesis . To our knowledge, the in vivo effects of SO or LA supplementation on macrophage atherogenicity have not been studied yet.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, consumption of at least 5–10% of energy as LA is recommended by the American Heart Association to reduce the risk of coronary heart disease (CHD) . Nevertheless, there have been conflicting reports regarding the role of SO or LA in CVD risk and atherogenesis, ranging from risk reduction, no effect, or increased risk . A meta‐analysis of prospective observational studies found that LA intake is inversely associated with CHD risk .…”

Section: Introductionmentioning

confidence: 99%

“…After differentiating from peripheral monocytes, the formed intimal macrophages incorporate oxidized/modified lipoproteins and are transformed into lipid‐rich foam cells, the hallmark feature of early atherosclerosis . In addition to lipoprotein uptake, lipid accumulation in macrophages can also result from alterations in cellular lipid metabolism, for example attenuated reverse lipid transport or enhanced rates of lipid biosynthesis . The atherosclerotic lesions and the macrophages isolated from those lesions contain not only cholesterol, but also a substantial amount of triglycerides .…”

Section: Introductionmentioning

confidence: 99%

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Supplementation with linoleic acid‐rich soybean oil stimulates macrophage foam cell formation via increased oxidative stress and diacylglycerol acyltransferase1‐mediated triglyceride biosynthesis

et al. 2016

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During the last decades there has been a staggering rise in human consumption of soybean oil (SO) and its major polyunsaturated fatty acid linoleic acid (LA). The role of SO or LA in cardiovascular diseases is highly controversial, and their impact on macrophage foam cell formation, the hallmark of early atherogenesis, is unclear. To investigate the effects of high SO or LA intake on macrophage lipid metabolism and the related mechanisms of action, C57BL/6 mice were orally supplemented with increasing levels of SO-based emulsion or equivalent levels of purified LA for 1 month, followed by analyses of lipid accumulation and peroxidation in aortas, serum and in peritoneal macrophages (MPM) of the mice. Lipid peroxidation and triglyceride mass in aortas from SO or LA supplemented mice were dose-dependently and significantly increased. In MPM from SO or LA supplemented mice, lipid peroxides were significantly increased and a marked accumulation of cellular triglycerides was found in accordance with enhanced triglyceride biosynthesis rate and overexpression of diacylglycerol acyltransferase1 (DGAT1), the key enzyme in triglyceride biosynthesis. In cultured J774A.1 macrophages treated with SO or LA, triglyceride accumulated via increased oxidative stress and a p38 mitogen-activated protein kinase (MAPK)-mediated overexpression of DGAT1. Accordingly, anti-oxidants (pomegranate polyphenols), inhibition of p38 MAPK (by SB202190) or DGAT1 (by oleanolic acid), all significantly attenuated SO or LA-induced macrophage triglyceride accumulation. These findings reveal novel mechanisms by which supplementation with SO or LA stimulate macrophage foam cell formation, suggesting a pro-atherogenic role for overconsumption of SO or LA. © 2016 BioFactors, 43(1):100-116, 2017.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Supplementation with linoleic acid‐rich soybean oil stimulates macrophage foam cell formation via increased oxidative stress and diacylglycerol acyltransferase1‐mediated triglyceride biosynthesis

et al. 2016

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“…A telí-tett zsírsavak fokozzák a LOX-1 expresszióját azáltal, hogy selejtes (misfolded) peptidek felhalmozódásával járó, úgynevezett endoplazmásreticulum-stresszt okoznak. A telítetlen zsírsavak ezzel szemben megelőzik a LOX-1 expresszióját a telített zsírsavakkal kezelt macrophagokban, és gátolják a LOX-1-upregulációt [13].…”

Section: Az Ldl-oxidáció Következményeiunclassified

“…Emellett az ox-LDL csökkenti a szöveti plazminogénaktivátor és növeli a plazminogénaktivátor inhibitor-1 aktivitását, ami az endothelium fi brinolitikus hatásának csökkenéséhez vezet. Összessé-gében ezek a folyamatok megmagyarázzák az elő rehaladott plakkok thromboticus szövődményeit [3,13].…”

Section: Az Ldl-oxidáció Következményeiunclassified

Oxidatív stressz és atherosclerosis

Stark

2015

Orvosi Hetilap

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Az atherosclerosis, ami a mai napig vezető halálok a fejlett országokban, genetikai hajlam és számos ismert környeze-ti rizikótényező hatására alakul ki. A legtöbb ilyen faktor oxidatív stressz keltése révén endothelialis működészavarhoz és egyéb proatherogen folyamatokhoz vezet. Az érelmeszesedés elsősorban az artériás rendszer tipikus helyein, az elágazásoknál és kanyarulatoknál alakul ki, ahol a szabályos lamináris áramlás zavart szenved. Emiatt fokozódik az endothelium permeabilitása a kis sűrűségű lipoprotein számára, ami így felhalmozódik az érfal intimarétegében és oxidálódik. Az oxidált kis sűrűségű lipoprotein számos úton hozzájárul az atherosclerosis kialakulásához: elősegíti a monocyták vándorlását az érfalba, a habossejt-képződést, a meszes plakk kialakulását, a plakkdestabilizációt és a thromboticus szövődményeket. Miután az oxidatív stressz az atherosclerosis patogenezisében számos ponton szerepet játszik, felmerül, hogy antioxidáns terápiával megelőzhető-e a betegség. Több klinikai vizsgálat szerint az antioxidánsok -mint az N-acetil-cisztein, C-és E-vitamin, folsav, ösztrogének -hatékonyak a coronariabetegség megelőzésében, de ezt randomizált klinikai vizsgálatok nem tudták bizonyítani. Orv. Hetil., 2015, 156(28), 1115-1119. Kulcsszavak: oxidatív stressz, érelmeszesedés, LDL-koleszterin, atheroscleroticus plakk, antioxidánsok Oxidative stress and atherosclerosisAtherosclerosis is a leading cause of death in developed countries. Genetic susceptibility and environmental factors play a role in the pathogenesis. Most of these factors lead to endothelial dysfunction and other pro-atherogenic processes by causing oxidative stress. Atherosclerosis typically develops at the curved and branched regions of the arterial tree, where the laminar blood fl ow is disturbed. This leads to increased permeability of the endothel to low density lipoprotein molecules, which accumulate in the intima and are oxidised by vascular cells. Oxidised low density lipoprotein takes part in many phases of atherogenesis: stimulates the binding of monocytes to the endothel, foam cell formation, the development of plaques, plaque destabilization and thrombotic complications. Since oxidative stress plays an important role in atherogenesis, it has been suggested that antioxidant molecules might have antiatherogenic function. Many clinical investigations have shown that antioxidants such as N-acetylcystein, vitamin E and C, folic acid, and estrogens can prevent atherosclerosis, however, randomized studies failed to confi rm this effect.Keywords: oxidative stress, atherosclerosis, LDL cholesterol, atherosclerotic plaque, antioxidants Stark, J. [Oxidative stress and atherosclerosis]. Orv. Hetil., 2015, 156(28), 1115-1119. (Beérkezett: 2015 elfogadva: 2015. május 22.) A közlemény a Fehér János Alapítvány pályázatán díjazott pályamunka. ÖSSZEFOGLALÓ KÖZLEMÉNYRövidítések ECM = extracelluláris mátrix; eNOS = endothelialis nitrogén-monoxid-szintáz; FGF = fi broblast növekedési faktor; ICAM-1 = intracelluláris adhéziós molekula-1; LOX-1...

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Conjugated linoleic acid (CLA) reduces HFD‐induced obesity by enhancing BAT thermogenesis and iWAT browning via the CD36–AMPK pathway

Zhang,

Fu,

Wang

et al. 2024

Cell Biochemistry & Function

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The antiobesity effect of conjugated linoleic acid (CLA) has been reported. However, the underlying mechanisms have not been fully clarified. Thus, this study aimed to investigate the effects of CLA on thermogenesis of interscapular brown adipose tissue (iBAT) and browning of inguinal subcutaneous white adipose tissue (iWAT) and explore the possible signaling pathway. The in vivo results showed that CLA enhanced the O2 consumption and heat production in HFD (high‐fat diet)‐fed female mice by roughly 38%. Meanwhile, CLA increased the average iBAT temperature by 2°C at the room temperature and cold exposure, respectively. Correspondingly, CLA caused 1.6‐ and 2.4‐fold increases in the expression of UCP1 (uncoupling protein 1) of BAT and iWAT, respectively, suggesting the activated iBAT thermogenesis and iWAT browning in HFD‐fed female mice. Meanwhile, CLA could promote the formation of brown and beige adipocytes in differentiated stromal vascular cells (SVCs) isolated from iBAT and iWAT (the expressions of UCP1 were promoted by about twofold changes). In possible mechanisms, CLA stimulated the expression of CD36 and the activation of the AMPK pathway in mice iBAT and iWAT as well as the differentiated SVCs. However, inhibition of CD36 and AMPK (adenosine 5′‐monophosphate‐activated protein kinase) abolished the promotive effects of CLA on brown and beige adipocytes formation. Hence, we showed that CLA reduced HFD‐induced obesity through enhancing iBAT thermogenesis and iWAT browning via the CD36–AMPK pathway.

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The impact of dietary fatty acids on macrophage cholesterol homeostasis

Cited by 30 publications

References 78 publications

Supplementation with linoleic acid‐rich soybean oil stimulates macrophage foam cell formation via increased oxidative stress and diacylglycerol acyltransferase1‐mediated triglyceride biosynthesis

Supplementation with linoleic acid‐rich soybean oil stimulates macrophage foam cell formation via increased oxidative stress and diacylglycerol acyltransferase1‐mediated triglyceride biosynthesis

Oxidatív stressz és atherosclerosis

Conjugated linoleic acid (CLA) reduces HFD‐induced obesity by enhancing BAT thermogenesis and iWAT browning via the CD36–AMPK pathway

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