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Castro M Cabezas - One of the best experts on this subject based on the ideXlab platform.
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effects of atorvastatin on fasting and postprandial Complement Component 3 response in familial combined hyperlipidemia
Journal of Lipid Research, 2003Co-Authors: C Verseyden, S Meijssen, H Van Dijk, Hans Jansen, Castro M CabezasAbstract:VLDL overproduction by enhanced hepatic FFA flux is a major characteristic of familial combined hyperlipidemia (FCHL). The postprandial Complement Component 3 (C3) response has been associated with impaired postprandial FFA metabolism in FCHL. We investigated the effects of 16 weeks of treatment with atorvastatin on postprandial C3 and lipid changes in 12 FCHL patients. Atorvastatin significantly lowered fasting plasma C3 and triglyceride (TG) in FCHL. Fasting TG and insulin sensitivity were the best predictors of fasting and postprandial C3. Postprandial triglyceridemia and C3 response, estimated as area under the curve (AUC), were significantly lowered by atorvastatin by 19% and 12%, respectively, albeit still elevated, compared with 10 matched controls. Postprandial FFA-AUC and postheparin plasma lipolytic activities remained unchanged after atorvastatin, suggesting no major effect on lipolysis. After atorvastatin, postprandial hydroxybutyric acid-AUC, which was elevated in untreated FCHL patients, was decreased, reaching values similar to those in controls. The present data show reduction of postprandial hepatic FFA flux in FCHL by atorvastatin, providing an additional mechanistic explanation for the reduction of VLDL secretion reported previously for atorvastatin. This was accompanied by a decrease in fasting plasma C3 concentrations and a blunted postprandial C3 response to an acute oral fat load.
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delayed and exaggerated postprandial Complement Component 3 response in familial combined hyperlipidemia
Arteriosclerosis Thrombosis and Vascular Biology, 2002Co-Authors: S Meijssen, H Van Dijk, C Verseyden, D W Erkelens, Castro M CabezasAbstract:Very low density lipoprotein overproduction is the major metabolic characteristic in familial combined hyperlipidemia (FCHL). Peripheral handling of free fatty acids (FFAs) in vitro may be impaired in FCHL by decreased action of acylation-stimulating protein (ASP), which is identical to the immunologically inactive Complement Component 3a (C3adesArg). Because decreased FFA uptake by impaired Complement Component 3 (C3) response (as the precursor for ASP) may result in enhanced FFA flux to the liver in FCHL, we have evaluated postprandial C3 changes in vivo in FCHL patients. Accordingly, 10 untreated FCHL patients and 10 matched control subjects underwent an oral fat loading test. Fasting plasma C3 and ASP levels were higher in FCHL patients (1.33+/-0.09 g/L and 70.53+/-4.37 mmol/L, respectively) than in control subjects (0.91+/-0.03 g/L and 43.21+/-8.96 mmol/L, respectively; P=0.01 and P<0.05). In control subjects, C3 concentrations increased significantly after 4 hours (to 1.03+/-0.04 g/L). In FCHL, plasma C3 was unchanged after 4 hours. The earliest postprandial C3 rise in FCHL patients occurred after 8 hours (1.64+/-0.12 g/L). The maximal apolipoprotein B-48 concentration was reached after 6 hours in FCHL patients and control subjects. Postprandial FFA and hydroxybutyric acid (as a marker of hepatic FFA oxidation) were significantly higher in FCHL patients than in control subjects, and the early postprandial C3 rise was negatively correlated with the postprandial FFA and hydroxybutyric acid concentrations. The present data suggest an impaired postprandial plasma C3 response in FCHL patients, most likely as a result of a delayed response by C3, as the precursor for the biologically active ASP, acting on FFA metabolism. Therefore, an impaired postprandial C3 response may be associated with impaired peripheral postprandial FFA uptake and, consequently, lead to increased hepatic FFA flux and very low density lipoprotein overproduction.
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postprandial increase of Complement Component 3 in normolipidemic patients with coronary artery disease effects of expanded dose simvastatin
Arteriosclerosis Thrombosis and Vascular Biology, 2001Co-Authors: C J M Halkes, H Van Dijk, D W Erkelens, P De Jaegere, H W M Plokker, Y J M Van Der Helm, Castro M CabezasAbstract:Plasma concentrations of the third Complement Component (C3) predict the risk of myocardial infarction. Because chylomicrons stimulate C3 production by adipocytes in vitro, we investigated plasma C3 changes in vivo after an oral fat load. Thirty-seven subjects (20 normolipidemic patients with coronary artery disease (CAD) and 17 healthy control subjects) underwent an oral fat load (50 g/m 2 ). C3 was measured at baseline and at 2-hour intervals after fat intake for 10 hours. The effects of lipid lowering by simvastatin were evaluated in 16 patients. Fasting plasma C3 was 1.0660.26 and 0.9060.12 g/L in CAD patients and control subjects, respectively. Fasting C3 was correlated with several parameters associated with insulin resistance. The best determinant of fasting C3 was waist circumference (adjusted R 2 50.48, b50.71, P,0.001); the addition of postprandial triglyceridemia to the model improved it (adjusted R 2 50.63). Plasma C3 levels at 2, 4, and 6 hours after fat ingestion were significantly higher than fasting levels in patients and control subjects. C3 increased maximally to 1.3960.33 g/L in patients and to 1.1160.18 g/L in control subjects (P,0.01 for patients versus control subjects). Total postprandial triglyceridemia was the best determinant of maximal C3 increase (adjusted R 2 50.47, b50.70; P,0.001). Treatment with simvastatin decreased fasting and postprandial C3 by 6% and 39%, respectively (P,0.05 for both versus no treatment). Postprandial plasma C3 concentrations increase in CAD patients and control subjects. Fasting C3 is associated with waist circumference, but postprandial C3 increment is associated with postprandial lipemia. Fasting and postprandial C3 concentrations decrease after treatment with simvastatin. (Arterioscler Thromb Vasc Biol. 2001;21:1526-1530.)
Ana Perezcastillo - One of the best experts on this subject based on the ideXlab platform.
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Complement Component 3 c3 expression in the hippocampus after excitotoxic injury role of c ebpβ
Journal of Neuroinflammation, 2016Co-Authors: Elena Hernandezencinas, Diana Aguilarmorante, Jose A Moralesgarcia, Elena Gine, Marina Sanzsancristobal, Angel Santos, Ana PerezcastilloAbstract:Background The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor implicated in the control of proliferation, differentiation, and inflammatory processes mainly in adipose tissue and liver; although more recent results have revealed an important role for this transcription factor in the brain. Previous studies from our laboratory indicated that CCAAT/enhancer-binding protein β is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. More recently, we have shown that the Complement Component 3 gene (C3) is a downstream target of CCAAT/enhancer-binding protein β and it could be a mediator of the proinflammatory effects of this transcription factor in neural cells.
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Complement Component 3 c3 expression in the hippocampus after excitotoxic injury role of c ebpβ
Journal of Neuroinflammation, 2016Co-Authors: Elena Hernandezencinas, Diana Aguilarmorante, Jose A Moralesgarcia, Elena Gine, Marina Sanzsancristobal, Angel Santos, Ana PerezcastilloAbstract:The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor implicated in the control of proliferation, differentiation, and inflammatory processes mainly in adipose tissue and liver; although more recent results have revealed an important role for this transcription factor in the brain. Previous studies from our laboratory indicated that CCAAT/enhancer-binding protein β is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. More recently, we have shown that the Complement Component 3 gene (C3) is a downstream target of CCAAT/enhancer-binding protein β and it could be a mediator of the proinflammatory effects of this transcription factor in neural cells. Adult male Wistar rats (8–12 weeks old) were used throughout the study. C/EBPβ+/+ and C/EBPβ–/– mice were generated from heterozygous breeding pairs. Animals were injected or not with kainic acid, brains removed, and brain slices containing the hippocampus analyzed for the expression of both CCAAT/enhancer-binding protein β and C3. In the present work, we have further extended these studies and show that CCAAT/enhancer-binding protein β and C3 co-express in the CA1 and CA3 regions of the hippocampus after an excitotoxic injury. Studies using CCAAT/enhancer-binding protein β knockout mice demonstrate a marked reduction in C3 expression after kainic acid injection in these animals, suggesting that indeed this protein is regulated by C/EBPβ in the hippocampus in vivo. Altogether these results suggest that CCAAT/enhancer-binding protein β could regulate brain disorders, in which excitotoxic and inflammatory processes are involved, at least in part through the direct regulation of C3.
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ccaat enhancer binding protein β directly regulates the expression of the Complement Component 3 gene in neural cells implications for the pro inflammatory effects of this transcription factor
Journal of Neuroinflammation, 2015Co-Authors: Elena Hernandezencinas, Diana Aguilarmorante, Jose A Moralesgarcia, Elena Gine, Angel Santos, Marta Cortescanteli, Ana PerezcastilloAbstract:The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor, which was first identified as a regulator of differentiation and inflammatory processes mainly in adipose tissue and liver; however, its function in the brain was largely unknown for many years. Previous studies from our laboratory indicated that C/EBPβ is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. We first performed cDNA microarrays analysis using hippocampal RNA isolated from C/EBPβ +/+ and C/EBPβ −/− mice. Immunocytochemical and immunohistochemical studies were done to evaluate C/EBPβ and C3 levels. Transient transfection experiments were made to analyze transcriptional regulation of C3 by C/EBPβ. To knockdown C/EBPβ and C3 expression, mouse astrocytes were infected with lentiviral particles expressing an shRNA specific for C/EBPβ or an siRNA specific for C3. Among the genes displaying significant changes in expression was Complement Component 3 (C3), which showed a dramatic decrease in mRNA content in the hippocampus of C/EBPβ −/− mice. C3 is the central Component of the Complement and is implicated in different brain disorders. In this work we have found that C/EBPβ regulates C3 levels in rodents glial in vitro and in the rat Substantia nigra pars compacta (SNpc) in vivo following an inflammatory insult. Analysis of the mouse C3 promoter showed that it is directly regulated by C/EBPβ through a C/EBPβ consensus site located at position −616/-599 of the gene. In addition, we show that depletion of C/EBPβ by a specific shRNA results in a significant decrease in the levels of C3 together with a reduction in the increased levels of pro-inflammatory agents elicited by lipopolysaccharide treatment. Altogether, these results indicate that C3 is a downstream target of C/EBPβ, and it could be a mediator of the pro-inflammatory effects of this transcription factor in neural cells.
C Verseyden - One of the best experts on this subject based on the ideXlab platform.
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addition of glucose to an oral fat load reduces postprandial free fatty acids and prevents the postprandial increase in Complement Component 3
The American Journal of Clinical Nutrition, 2004Co-Authors: Antonie J H H M Van Oostrom, C Verseyden, Hans Van Dijk, Allan D Sniderman, Katherine Cianflone, Ton J Rabelink, Manuel Castro CabezasAbstract:Background: Elevated fasting plasma concentrations of Complement Component 3 (C3) are associated with elevated fasting and postprandial triacylglycerol concentrations, insulin resistance, obesity, and coronary artery disease. C3 is the central Component of the Complement system and the precursor of acylation-stimulating protein (ASP). Insulin and ASP are principal determinants of free fatty acid (FFA) trapping by adipose tissue. Objective: Because controversy exists concerning postprandial changes in C3 and because meal composition may influence Complement activation, we studied postprandial lipemia in relation to changes in plasma C3. Design: After an overnight fast, 6 healthy men (x SD age: 23 2 y) underwent 4 oral liquid challenges: fat (50 g/m 2 body surface), glucose (37.5 g/m 2 ), fat and glucose (mixed test), and water (as a control test) in a random, crossover design. Results: Plasma ASP concentrations did not change postprandially in any test. Changes in C3 concentration were observed only after the fat challenge: elevated concentrations occurred between 1 and 3 h, and a maximum increase of 11% occurred at 2 h (P 0.05). Postprandial triacylglycerolemia did not differ significantly between the fat and mixed tests. The FFA response after the fat challenge was the highest of all the tests (P 0.05 for all comparisons) and was accompanied by an increase in ketone bodies (maximum at 6 h); this increase did not occur after the mixed test, which suggests less hepatic FFA delivery. Conclusions: When glucose is added to an oral fat load, the postprandial FFA response is reduced, and the fat-specific increase in C3 is prevented. After ingestion of fat without glucose, the lack of insulin response may lead to C3-mediated peripheral FFA trapping, which probably serves as a backup system in case of insufficient or inefficient insulin-dependent FFA trapping. Am J Clin Nutr 2004;79:510 –5.
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effects of atorvastatin on fasting and postprandial Complement Component 3 response in familial combined hyperlipidemia
Journal of Lipid Research, 2003Co-Authors: C Verseyden, S Meijssen, H Van Dijk, Hans Jansen, Castro M CabezasAbstract:VLDL overproduction by enhanced hepatic FFA flux is a major characteristic of familial combined hyperlipidemia (FCHL). The postprandial Complement Component 3 (C3) response has been associated with impaired postprandial FFA metabolism in FCHL. We investigated the effects of 16 weeks of treatment with atorvastatin on postprandial C3 and lipid changes in 12 FCHL patients. Atorvastatin significantly lowered fasting plasma C3 and triglyceride (TG) in FCHL. Fasting TG and insulin sensitivity were the best predictors of fasting and postprandial C3. Postprandial triglyceridemia and C3 response, estimated as area under the curve (AUC), were significantly lowered by atorvastatin by 19% and 12%, respectively, albeit still elevated, compared with 10 matched controls. Postprandial FFA-AUC and postheparin plasma lipolytic activities remained unchanged after atorvastatin, suggesting no major effect on lipolysis. After atorvastatin, postprandial hydroxybutyric acid-AUC, which was elevated in untreated FCHL patients, was decreased, reaching values similar to those in controls. The present data show reduction of postprandial hepatic FFA flux in FCHL by atorvastatin, providing an additional mechanistic explanation for the reduction of VLDL secretion reported previously for atorvastatin. This was accompanied by a decrease in fasting plasma C3 concentrations and a blunted postprandial C3 response to an acute oral fat load.
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delayed and exaggerated postprandial Complement Component 3 response in familial combined hyperlipidemia
Arteriosclerosis Thrombosis and Vascular Biology, 2002Co-Authors: S Meijssen, H Van Dijk, C Verseyden, D W Erkelens, Castro M CabezasAbstract:Very low density lipoprotein overproduction is the major metabolic characteristic in familial combined hyperlipidemia (FCHL). Peripheral handling of free fatty acids (FFAs) in vitro may be impaired in FCHL by decreased action of acylation-stimulating protein (ASP), which is identical to the immunologically inactive Complement Component 3a (C3adesArg). Because decreased FFA uptake by impaired Complement Component 3 (C3) response (as the precursor for ASP) may result in enhanced FFA flux to the liver in FCHL, we have evaluated postprandial C3 changes in vivo in FCHL patients. Accordingly, 10 untreated FCHL patients and 10 matched control subjects underwent an oral fat loading test. Fasting plasma C3 and ASP levels were higher in FCHL patients (1.33+/-0.09 g/L and 70.53+/-4.37 mmol/L, respectively) than in control subjects (0.91+/-0.03 g/L and 43.21+/-8.96 mmol/L, respectively; P=0.01 and P<0.05). In control subjects, C3 concentrations increased significantly after 4 hours (to 1.03+/-0.04 g/L). In FCHL, plasma C3 was unchanged after 4 hours. The earliest postprandial C3 rise in FCHL patients occurred after 8 hours (1.64+/-0.12 g/L). The maximal apolipoprotein B-48 concentration was reached after 6 hours in FCHL patients and control subjects. Postprandial FFA and hydroxybutyric acid (as a marker of hepatic FFA oxidation) were significantly higher in FCHL patients than in control subjects, and the early postprandial C3 rise was negatively correlated with the postprandial FFA and hydroxybutyric acid concentrations. The present data suggest an impaired postprandial plasma C3 response in FCHL patients, most likely as a result of a delayed response by C3, as the precursor for the biologically active ASP, acting on FFA metabolism. Therefore, an impaired postprandial C3 response may be associated with impaired peripheral postprandial FFA uptake and, consequently, lead to increased hepatic FFA flux and very low density lipoprotein overproduction.
Yun Seon Song - One of the best experts on this subject based on the ideXlab platform.
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neuroprotective effect of mesenchymal stem cell through Complement Component 3 downregulation after transient focal cerebral ischemia in mice
Neuroscience Letters, 2016Co-Authors: Hyeseon Jung, Jiwon Yang, Siyeon Jeong, Sodam Kim, Baojin Zhang, Hyun Seung Yoo, Sun U Song, Myungshin Jeon, Yun Seon SongAbstract:Bone marrow-derived mesenchymal stem cells (MSCs) are used in stroke treatment despite the poor understanding of its mode of action. The immune suppressive and anti-inflammatory properties of MSCs possibly play important roles in regulating neuroinflammation after stroke. We investigated whether MSCs reduce the inflammatory Complement Component 3 (C3) levels, thus, providing neuroprotection during stroke. Mice were subjected to transient focal cerebral ischemia (tFCI), after which MSCs were intravenously injected. The infarct volume of the brain was reduced in MSC-injected tFCI mice, and C3 expression was significantly reduced in both the brain and the blood. Additionally, the profiles of other inflammatory mediators demonstrated neuroprotective changes in the MSCs-treated group. In order to analyze the effect of MSCs on neurons during cerebral ischemia, primary cortical neurons were co-cultured with MSCs under oxygen-glucose deprivation (OGD). Primary neurons co-cultured with MSCs exhibited reduced levels of C3 expression and increased protection against OGD, indicating that treatment with MSCs reduces excessive C3 expression and rescues ischemia-induced neuronal damage. Our finding suggests that reduction of C3 expression by MSCs can help to ameliorate ischemic brain damage, offering a new neuroprotective strategy in stroke therapy.
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Complement Component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice
Journal of Neurochemistry, 2013Co-Authors: Jiwon Yang, Hyena Ahn, Minsun Chang, Purnima Narasimhan, Pak H Chan, Yun Seon SongAbstract:Oxidative stress after stroke is associated with the inflammatory system activation in the brain. The Complement cascade, especially the degradation products of Complement Component 3, is a key inflammatory mediator of cerebral ischemia. We have shown that pro-inflammatory Complement Component 3 is increased by oxidative stress after ischemic stroke in mice using DNA array. In this study, we investigated whether up-regulation of Complement Component 3 is directly related to oxidative stress after transient focal cerebral ischemia in mice and oxygen-glucose deprivation in brain cells. Persistent up-regulation of Complement Component 3 expression was reduced in copper/zinc-superoxide dismutase transgenic mice, and manganese-superoxide dismutase knock-out mice showed highly increased Complement Component 3 levels after transient focal cerebral ischemia. Antioxidant N-tert-butyl-α-phenylnitrone treatment suppressed Complement Component 3 expression after transient focal cerebral ischemia. Accumulation of Complement Component 3 in neurons and microglia was decreased by N-tert-butyl-α-phenylnitrone, which reduced infarct volume and impaired neurological deficiency after cerebral ischemia and reperfusion in mice. Small interfering RNA specific for Complement Component 3 transfection showed a significant increase in brain cells viability after oxygen-glucose deprivation. Our study suggests that the neuroprotective effect of antioxidants through Complement Component 3 suppression is a new strategy for potential therapeutic approaches in stroke.
H Van Dijk - One of the best experts on this subject based on the ideXlab platform.
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effects of atorvastatin on fasting and postprandial Complement Component 3 response in familial combined hyperlipidemia
Journal of Lipid Research, 2003Co-Authors: C Verseyden, S Meijssen, H Van Dijk, Hans Jansen, Castro M CabezasAbstract:VLDL overproduction by enhanced hepatic FFA flux is a major characteristic of familial combined hyperlipidemia (FCHL). The postprandial Complement Component 3 (C3) response has been associated with impaired postprandial FFA metabolism in FCHL. We investigated the effects of 16 weeks of treatment with atorvastatin on postprandial C3 and lipid changes in 12 FCHL patients. Atorvastatin significantly lowered fasting plasma C3 and triglyceride (TG) in FCHL. Fasting TG and insulin sensitivity were the best predictors of fasting and postprandial C3. Postprandial triglyceridemia and C3 response, estimated as area under the curve (AUC), were significantly lowered by atorvastatin by 19% and 12%, respectively, albeit still elevated, compared with 10 matched controls. Postprandial FFA-AUC and postheparin plasma lipolytic activities remained unchanged after atorvastatin, suggesting no major effect on lipolysis. After atorvastatin, postprandial hydroxybutyric acid-AUC, which was elevated in untreated FCHL patients, was decreased, reaching values similar to those in controls. The present data show reduction of postprandial hepatic FFA flux in FCHL by atorvastatin, providing an additional mechanistic explanation for the reduction of VLDL secretion reported previously for atorvastatin. This was accompanied by a decrease in fasting plasma C3 concentrations and a blunted postprandial C3 response to an acute oral fat load.
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delayed and exaggerated postprandial Complement Component 3 response in familial combined hyperlipidemia
Arteriosclerosis Thrombosis and Vascular Biology, 2002Co-Authors: S Meijssen, H Van Dijk, C Verseyden, D W Erkelens, Castro M CabezasAbstract:Very low density lipoprotein overproduction is the major metabolic characteristic in familial combined hyperlipidemia (FCHL). Peripheral handling of free fatty acids (FFAs) in vitro may be impaired in FCHL by decreased action of acylation-stimulating protein (ASP), which is identical to the immunologically inactive Complement Component 3a (C3adesArg). Because decreased FFA uptake by impaired Complement Component 3 (C3) response (as the precursor for ASP) may result in enhanced FFA flux to the liver in FCHL, we have evaluated postprandial C3 changes in vivo in FCHL patients. Accordingly, 10 untreated FCHL patients and 10 matched control subjects underwent an oral fat loading test. Fasting plasma C3 and ASP levels were higher in FCHL patients (1.33+/-0.09 g/L and 70.53+/-4.37 mmol/L, respectively) than in control subjects (0.91+/-0.03 g/L and 43.21+/-8.96 mmol/L, respectively; P=0.01 and P<0.05). In control subjects, C3 concentrations increased significantly after 4 hours (to 1.03+/-0.04 g/L). In FCHL, plasma C3 was unchanged after 4 hours. The earliest postprandial C3 rise in FCHL patients occurred after 8 hours (1.64+/-0.12 g/L). The maximal apolipoprotein B-48 concentration was reached after 6 hours in FCHL patients and control subjects. Postprandial FFA and hydroxybutyric acid (as a marker of hepatic FFA oxidation) were significantly higher in FCHL patients than in control subjects, and the early postprandial C3 rise was negatively correlated with the postprandial FFA and hydroxybutyric acid concentrations. The present data suggest an impaired postprandial plasma C3 response in FCHL patients, most likely as a result of a delayed response by C3, as the precursor for the biologically active ASP, acting on FFA metabolism. Therefore, an impaired postprandial C3 response may be associated with impaired peripheral postprandial FFA uptake and, consequently, lead to increased hepatic FFA flux and very low density lipoprotein overproduction.
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postprandial increase of Complement Component 3 in normolipidemic patients with coronary artery disease effects of expanded dose simvastatin
Arteriosclerosis Thrombosis and Vascular Biology, 2001Co-Authors: C J M Halkes, H Van Dijk, D W Erkelens, P De Jaegere, H W M Plokker, Y J M Van Der Helm, Castro M CabezasAbstract:Plasma concentrations of the third Complement Component (C3) predict the risk of myocardial infarction. Because chylomicrons stimulate C3 production by adipocytes in vitro, we investigated plasma C3 changes in vivo after an oral fat load. Thirty-seven subjects (20 normolipidemic patients with coronary artery disease (CAD) and 17 healthy control subjects) underwent an oral fat load (50 g/m 2 ). C3 was measured at baseline and at 2-hour intervals after fat intake for 10 hours. The effects of lipid lowering by simvastatin were evaluated in 16 patients. Fasting plasma C3 was 1.0660.26 and 0.9060.12 g/L in CAD patients and control subjects, respectively. Fasting C3 was correlated with several parameters associated with insulin resistance. The best determinant of fasting C3 was waist circumference (adjusted R 2 50.48, b50.71, P,0.001); the addition of postprandial triglyceridemia to the model improved it (adjusted R 2 50.63). Plasma C3 levels at 2, 4, and 6 hours after fat ingestion were significantly higher than fasting levels in patients and control subjects. C3 increased maximally to 1.3960.33 g/L in patients and to 1.1160.18 g/L in control subjects (P,0.01 for patients versus control subjects). Total postprandial triglyceridemia was the best determinant of maximal C3 increase (adjusted R 2 50.47, b50.70; P,0.001). Treatment with simvastatin decreased fasting and postprandial C3 by 6% and 39%, respectively (P,0.05 for both versus no treatment). Postprandial plasma C3 concentrations increase in CAD patients and control subjects. Fasting C3 is associated with waist circumference, but postprandial C3 increment is associated with postprandial lipemia. Fasting and postprandial C3 concentrations decrease after treatment with simvastatin. (Arterioscler Thromb Vasc Biol. 2001;21:1526-1530.)