2002
DOI: 10.1023/a:1020538119691
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Abstract: Despite decades of extensive research, the transport routes, mechanisms of uptake and points of flux control of long-chain fatty acids (FA) in mammalian organs are still incompletely understood. In non-fenestratred organs such as heart and skeletal muscle, membrane barriers for blood-borne FA are the luminal and abluminal membranes of endothelial cells, the sarcolemma and the mitochondrial membranes. Transport of FA through the phospholipid bilayer of the cellular membrane is most likely accomplished by diffus… Show more

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Cited by 61 publications
(20 citation statements)
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“…Analysis using qRT-PCR showed no difference in key transcripts from the major pathways implicated in the development of NAFLD comparing experimental and control animals (Table S1) [31], [32], [33], [34], [35], [36]. To gain further insight into the pathogenesis of NAFLD in the ICD-E mice we therefore examined liver transcription at 6 and 24 hour time points, using expression microarrays.…”
Section: Resultsmentioning
confidence: 99%
“…Analysis using qRT-PCR showed no difference in key transcripts from the major pathways implicated in the development of NAFLD comparing experimental and control animals (Table S1) [31], [32], [33], [34], [35], [36]. To gain further insight into the pathogenesis of NAFLD in the ICD-E mice we therefore examined liver transcription at 6 and 24 hour time points, using expression microarrays.…”
Section: Resultsmentioning
confidence: 99%
“…The intensity of FFA uptake by myocardial cells is determined by their plasma concentrations. Excess products and metabolites of FFA oxidation (acetyl-CoA, reduced NADPH, and FAD2) are natural inhibitors of pyruvate dehydrogenase complex enzymes, responsible for aerobic glucose oxidation, which leads to a decrease in myocardial glucose use [12]. In ischemia, the main metabolic pathway providing energy to cardiomyocytes is anerobic glycolysis because FFA oxidation requires more oxygen.…”
Section: Discussionmentioning
confidence: 99%
“…An elevation of FFAs would increase their uptake/transport and metabolism in BAECs. It is generally recognized that FFAs can enter ECs by passive diffusion, which is facilitated by the membrane fatty acid-binding protein but reduced by the presence of albumin (Goresky et al 1994, Burczynski et al 1995, van der Vusse et al 2002. An increased incorporation of FFAs into ECs would alter the metabolic pathways, including possible uncoupling of oxidative phosphorylation and reduction of ROS formation in mitochondria.…”
Section: Cmentioning
confidence: 99%
“…It is possible that FFAs, similar to hyperglycemia, cause damage to ECs by overproduction of superoxide by the mitochondrial electron transport chain, leading to dysfunction in other metabolic pathways (Brownlee 2005, Du et al 2006, Imrie et al 2010. Infusion of FFAs reduced endothelium-dependent vasodilation in animal models and in humans in vivo (Davda et al 1995, Steinberg et al 2000, Pleiner et al 2002, Tripathy et al 2003 and co-infusion of the antioxidant ascorbic acid improved endothelium-dependent vasodilation (Pleiner et al 2002), indicating that oxidative stress might mediate the abnormality. Indeed, co-culture with antioxidants, in our study, was able to largely reverse the impairing effects of high FFAs on NO production and related signaling events in ECs.…”
Section: Cmentioning
confidence: 99%
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