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Relevant bibliographies by topics / Apolipoprotien C III

Academic literature on the topic 'Apolipoprotien C III'

Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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Journal articles on the topic "Apolipoprotien C III"

1

Puchois, P., C. Luley, and P. Alaupovic. "Comparison of four procedures for separating apolipoprotein A- and apolipoprotein B-containing lipoproteins in plasma." Clinical Chemistry 33, no. 9 (September 1, 1987): 1597–602. http://dx.doi.org/10.1093/clinchem/33.9.1597.

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Abstract Because lipoproteins containing apolipoprotein A (ApoA-I + ApoA-II) or apolipoprotein B (ApoB) seem to exert opposite effects as risk factors for coronary heart disease, we decided to determine the separability of these two major plasma lipoproteins by procedures originally designed to separate high-density from low- and very-low-density lipoproteins. The presumably ApoB-free lipoproteins isolated from normal plasma by (a) ultracentrifugation at d = 1.063; precipitation with (b) heparin-Mn2+ or (c) phosphotungstate-Mg2+; or (d) immunoprecipitation with antibodies to ApoB were characterized by quantifying cholesterol and apolipoproteins A-I, A-II, B, C-II, C-III, D, E, F, and Lp(a). ApoA- and ApoB-containing lipoproteins were completely separated only by immunoprecipitation with antibodies to ApoB. The ApoB-containing lipoproteins isolated by other procedures always contained 4% to 20% of total plasma ApoA-I and differed substantially from one another with respect to the content of some of the minor apolipoproteins. Measuring apolipoproteins was more reliable than measuring cholesterol for monitoring this separation and for expressing the concentrations of ApoA- and ApoB-containing lipoproteins.

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2

März, W., G. Schenk, and W. Gross. "Apolipoproteins C-II and C-III in serum quantified by zone immunoelectrophoresis." Clinical Chemistry 33, no. 5 (May 1, 1987): 664–69. http://dx.doi.org/10.1093/clinchem/33.5.664.

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Abstract Zone immunoelectrophoresis assays specific for apolipoprotein C-II and C-III have been developed. These simple, accurate, reproducible, and sensitive methods present valid alternatives to conventional immunoassays. In fasting normolipidemic men and women the concentrations of apolipoprotein C-II and C-III were 49 (SD 25) mg/L and 124 (SD 60) mg/L, respectively, with no sex-related differences for either apolipoprotein. The frequency distribution of apolipoprotein C-II was skewed to the right, whereas apolipoprotein C-III was bimodally distributed. Concentrations of each apolipoprotein correlated well with one another and with that of serum triglycerides, but there was virtually no correlation between the apolipoprotein C-II to C-III mass ratio and the concentration of triglycerides. Apolipoprotein C-III, but not apolipoprotein C-II, was statistically associated with total cholesterol.

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Visvikis, S., M. F. Dumon, J. Steinmetz, T. Manabe, M. M. Galteau, M. Clerc, and G. Siest. "Plasma apolipoproteins in Tangier disease, as studied with two-dimensional electrophoresis." Clinical Chemistry 33, no. 1 (January 1, 1987): 120–22. http://dx.doi.org/10.1093/clinchem/33.1.120.

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Abstract Tangier disease is characterized by a deficiency of high-density lipoproteins and of their major protein constituent, apolipoprotein (apo) A-I. We used high-resolution two-dimensional electrophoresis to examine the principal plasma apolipoproteins (A-I, A-II, A-IV, E, C-II, and C-III) of three persons with Tangier disease, one homozygous patient and his two heterozygous children, comparing the patterns with those for healthy subjects. Characteristic abnormalities were found in the distribution of the isoproteins of apo A-I, there being a normal concentration of pro apo A-I but dramatically decreased concentrations of the other apo A-I isoproteins. We also found hitherto-undescribed polypeptide abnormalities in apo C-III: sialylated and nonsialylated forms of apo C-III appear as double spots having the same isoelectric points but different molecular masses. No other substantial difference was detected in the polypeptide distribution of the other plasma apolipoproteins.

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Hata, M., T. Ito, and K. Ohwada. "Kinetic analysis of apolipoproteins in postprandial hypertriglyceridaemia rabbits." Laboratory Animals 43, no. 2 (April 2009): 174–81. http://dx.doi.org/10.1258/la.2008.007004.

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The postprandial hypertriglyceridaemia (PHT) rabbit, developed as a new animal model of metabolic syndrome, is characterized by PHT, central obesity and glucose intolerance. For detailed investigation of lipid metabolism characteristics in PHT rabbit, the plasma levels of apolipoproteins A-I, B, C-II, C-III and E were measured. Movements of apolipoproteins B100 and B48 were investigated using sodium dodecyl sulphate–polyacrylamide gel electrophoresis to determine whether postprandially increased triglyceride is exogenous or endogenous. The level of apolipoproteins A-I, B, C-II and E were increased in PHT rabbit after feeding. Apolipoproteins B100 and B48 were detected in the plasma fraction of d < 1.006 g/mL of the PHT rabbit. The postprandial increase in apolipoprotein B in the PHT rabbit reflects a numerical increase in lipoprotein particles in the blood; the increase in apolipoproteins C-II and E suggests some disturbance in lipoprotein catabolism. Apolipoprotein B48 was detected postprandially in PHT rabbits. These results suggest that delayed catabolism of exogenous lipids caused the retention of chylomicron remnants in the blood. Results also suggest that activities of the lipolytic enzyme lipoprotein lipase and hepatic triglyceride lipase were deficient and that the hepatic uptake of exogenous lipoproteins was delayed in the PHT rabbit. Especially, for examining remnant hyperlipoproteinaemia in humans, PHT rabbit is an excellent animal model for hypertriglyceridaemia research.

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Miller, Michael. "Apolipoprotein C-III." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 6 (June 2017): 1013–14. http://dx.doi.org/10.1161/atvbaha.117.309493.

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Huff, Murray W., and Robert A. Hegele. "Apolipoprotein C-III." Circulation Research 112, no. 11 (May 24, 2013): 1405–8. http://dx.doi.org/10.1161/circresaha.113.301464.

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7

Kohan, Alison B. "Apolipoprotein C-III." Current Opinion in Endocrinology & Diabetes and Obesity 22, no. 2 (April 2015): 119–25. http://dx.doi.org/10.1097/med.0000000000000136.

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Wang, Wenyu, Piers Blackett, Sohail Khan, and Elisa Lee. "Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee." Journal of Lipids 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/8236325.

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Since young adult Cherokee are at increased risk for both diabetes and cardiovascular disease, we assessed association of apolipoproteins (A-I, B, and C-III in non-HDL and HDL) with obesity and related risk factors. Obese participants (BMI ≥ 30) aged 20–40 years (n=476) were studied. Metabolically healthy obese (MHO) individuals were defined as not having any of four components of the ATP-III metabolic syndrome after exclusion of waist circumference, and obese participants not being MHO were defined as metabolically abnormal obese (MAO). Associations were evaluated by correlation and regression modeling. Obesity measures, blood pressure, insulin resistance, lipids, and apolipoproteins were significantly different between groups except for total cholesterol, LDL-C, and HDL-apoC-III. Apolipoproteins were not correlated with obesity measures with the exception of apoA-I with waist and the waist : height ratio. In a logistic regression model apoA-I and the apoB : apoA-I ratio were significantly selected for identifying those being MHO, and the result (C-statistic = 0.902) indicated that apoA-I and the apoB : apoA-I ratio can be used to identify a subgroup of obese individuals with a significantly less atherogenic lipid and apolipoprotein profile, particularly in obese Cherokee men in whom MHO is more likely.

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Huet, G., M. C. Dieu, A. Martin, G. Grard, J. M. Bard, P. Fossati, and P. Degand. "Heterozygous hypobetalipoproteinemia with fasting chylomicronemia." Clinical Chemistry 37, no. 2 (February 1, 1991): 296–300. http://dx.doi.org/10.1093/clinchem/37.2.0296.

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Abstract We describe a disorder in which low-density lipoprotein (LDL)-cholesterol and apolipoprotein B are in low concentration (0.47 mmol/L and 0.28 g/L, respectively) and chylomicrons are still present in plasma after an 18-h fast. The d less than 1.006 fraction was isolated by flotation ultracentrifugation and the apolipoproteins were analyzed by electrophoresis, immunoblotting with anti-apolipoprotein B-100 antiserum, and isoelectric focusing. In the d less than 1.006 fraction of the fasting serum, we found an apolipoprotein B form with the same apparent molecular mass as apolipoprotein B-48 and similar in amount to apolipoprotein B-100 (respective percentages, 46% and 54%). The monosialylated form of the apolipoprotein C-III was severely decreased. After an oral fat load, the repartition of the two species of apolipoprotein B did not change greatly (respective percentages, 60% and 40%), and the concentration of serum triglyceride increased only from 1.20 to 1.65 mmol/L.

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Wang, C. S., W. J. McConathy, H. U. Kloer, and P. Alaupovic. "Modulation of lipoprotein lipase activity by apolipoproteins. Effect of apolipoprotein C-III." Journal of Clinical Investigation 75, no. 2 (February 1, 1985): 384–90. http://dx.doi.org/10.1172/jci111711.

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Dissertations / Theses on the topic "Apolipoprotien C III"

1

Clabé, Alain. "Apolipoprotéines C-II, C-III et E : mise au point et essai d'une technique de dosage immunonéphélémétrique." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2P028.

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SEFRAOUI, MOHAMMED. "Les apolipoproteines a-iv, cii, c-iii et e : polymorphisme des apolipoproteines a-iv et e, quantification des apolipoproteines c-ii et c-iii o-2 chez les sujets hyperlipoproteinemiques." Lille 2, 1989. http://www.theses.fr/1989LIL2P262.

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Mauger, Jean-François. "Apolipoptotéine C-III, taille des LDL et protéine C-réactive." Doctoral thesis, Université Laval, 2009. http://hdl.handle.net/20.500.11794/20954.

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Le syndrome métabolique est un regroupement de facteurs de nsque de maladie cardiovasculaire (MCV) étroitement liés à l'obésité. L 'hypertriglycéridémie, la présence en circulation de lipoprotéines de faible densité (LDL) de diamètre réduit et une condition proinflammatoire représentent trois de ces facteurs. L' apoliprotéine (apo) C-III, présente sous 3 isoformes en circulation, inhibe la lipase lipoprotéique. et serait impliquée dans le développement de l 'hypertriglycéridémie. Les LDL petites et denses seraient métabolisées moins rapidement et seraient ' ainsi plus susceptibles de participer au processus athérosclérotique. Les concentrations plasmatiques élevées de protéine C-réactive (CRP) sont utilisées en clinique dans l'évaluation de la condition inflammatoire et dans l'estimation du profil de risque de MCV. La compréhension du métabolisme intravasculair-e de l'apoC-III, des différentes classes de LDL et de la CRP en rapport avec le syndrome métabolique est incomplète. Utilisant des techniques de traçage in vivo, les mécanismes physiologiques (taux de production et de catabolisme) responsables des variations de concentrations plasmatiques des différents isoformes de l'apoC-III, de la CRP et des LDL petites et denses furent étudiés. Les études sur le métabolisme intravasculaire de l' apoC-III ont démontré que le taux de production de l'ensemble des isoformes de l' apoC-III était positivement associé aux concentrations plasmatiques de triglycérides et que le taux de production de l'isoforme doublement sialylée était fortement associé à la proportion de petites LDL en circulation. L'étude de la cinétique intravasculaire de différentes sousclasses de LDL a révélé que les LDL de moindres densités, malgré ' leur métabolisme intravasculaire rapide, sont les principaux précurseurs des LDL de plus hautes densités. Finalement, l'étude de la CRP révéla que les concentrations plasmatiques de ce marqueur inflammatoire sont déterminées principalement par son taux de production, et que ce dernier serait positivement associé au tour de taille et aux concentrations plasmatiques d'apoB-lOOet de triglycérides, et négativement associé aux concentrations plasmatiques de lipoprotéines de haute densité et d'adiponectine. Dans l'ensemble, ces études in vivo auront permis de mieux situer le rôle métabolique des isoformes de l'apoC-III, des LDL et de la CRP dans le développement du syndrome métabolique et appellent à la réalisation d'études dans divers contextes métaboliques afin de valider les conclusions ici présentées.

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CANDELIER, LAURENT. "Isolement et caracterisation des particules lipoproteiques plasmatiques lpb, lpb : e, lpb c-iii et lpb : c-iii : e. mise au point et utilisation d'une methode de chromatographie d'immunoaffinite sequentielle." Lille 2, 1989. http://www.theses.fr/1989LIL2P259.

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Mauger, Jean-François. "Apolipoprotéine C-III, taille des LDL et protéine C-réactive. Études physiologiques en relation avec le syndrome métabolique." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26400/26400.pdf.

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Koska, Juraj, Hussein Yassine, Olgica Trenchevska, Shripad Sinari, Dawn C. Schwenke, Frances T. Yen, Dean Billheimer, Randall W. Nelson, Dobrin Nedelkov, and Peter D. Reaven. "Disialylated apolipoprotein C-III proteoform is associated with improved lipids in prediabetes and type 2 diabetes." AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2016. http://hdl.handle.net/10150/614755.

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The apoC-III proteoform containing two sialic acid residues (apoC-III2) has different in vitro effects on lipid metabolism compared with asialylated (apoC-III0) or the most abundant monosialylated (apoC-III1) proteoforms. Cross-sectional and longitudinal associations between plasma apoC-III proteoforms (by mass spectrometric immunoassay) and plasma lipids were tested in two randomized clinical trials: ACT NOW, a study of pioglitazone in subjects with impaired glucose tolerance (n = 531), and RACED (n = 296), a study of intensive glycemic control and atherosclerosis in type 2 diabetes patients. At baseline, higher relative apoC-(I)II2 and apoC-III2/apoC-III1 ratios were associated with lower triglycerides and total cholesterol in both cohorts, and with lower small dense LDL in the RACED. Longitudinally, changes in apoC-III2/apoC-III1 were inversely associated with changes in triglycerides in both cohorts, and with total and small dense LDL in the RACED. apoC-III2/apoC-III1 was also higher in patients treated with PPAR-gamma agonists and was associated with reduced cardiovascular events in the RACED control group. Ex vivo studies of apoC-III complexes with higher apoC-III2/apoC-III1 showed attenuated inhibition of VLDL uptake by HepG2 cells and LPL-mediated lipolysis, providing possible functional explanations for the inverse association between a higher apoC-III2/apoC-III1 and hypertriglyceridemia, proatherogenic plasma lipid profiles, and cardiovascular risk.

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Ellena, Rachel A. "Antimicrobial and lipid binding properties of the C-terminal domain of apolipoprotein A-I determined using a novel apolipophorin III/apolipoprotein A-I (179-243) chimera." Thesis, California State University, Long Beach, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10144827.

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Apolipoprotein A-I (apoA-I) is an exchangeable apolipoprotein that constitutes the major protein component of high density cholesterol. ApoA-I is a two-domain protein comprising an N-terminal helix bundle and a less-structured C-terminal domain in the lipid-free state. In the present study, the contribution of the C-terminal domain to the lipid binding and antimicrobial activity of apoA-I was investigated using a chimeric construct in which the C-terminal domain of apoA-I (179-243) was attached to an insect apolipoprotein, Locusta migratoria apolipophorin III (apoLp-III), bearing cysteine substitutions for residues 20 and 149. Circular dichroism results were consistent with the addition of a poorly structured domain to apoLp-III and revealed the apoLp-III helix bundle was successfully closed under oxidizing conditions. Electrophoresis, fluorescence spectroscopy and an in vitro study using macrophage cells revealed that the C-terminal domain in itself was insufficient for efficient binding to lipid, lipopolysaccharide and phosphatidylglycerol vesicles. These results suggest the underlying mechanisms governing these interactions are potentiated by cooperativity between the N- and C-terminal domains of apoA-I.

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Pan, Wenru. "Triglyceride rich lipoproteins and Apolipoprotein C-III in Atherosclerosis." Thesis, 2020. http://hdl.handle.net/2440/129639.

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While the causal role of low-density lipoprotein cholesterol (LDL-C) in atherosclerosis and the clinical benefit of lipid lowering with statins are well established, the impact of triglyceride rich lipoproteins (TRL) in cardiovascular disease is less well understood. Given the important association between hypertriglyceridaemia and both obesity and type 2 diabetes, mechanistic studies are required to further understand the role of TRL as both a causal factor and potential target for therapeutic modification. This thesis aims to investigate the impact of both TRL and Apolipoprotein C-III (ApoC-III), an important factor that regulates TRL metabolism, in atherosclerosis. It demonstrated the adverse effect of oxidised TRL on endothelial cells following co-incubation studies in vitro. It also described the presence of ApoC-III within atherosclerotic lesions in an animal model of diabetes and dyslipidaemia, with evidence of a direct correlation between plaque levels of ApoC-III with both the burden and inflammatory composition of plaques. Additional studies demonstrated inverse correlations between hepatic levels of triglyceride and ApoC-III with expression of factors involved in the generation of high-density liporptoeins (HDL) and the promotion of reverse cholesterol transport. Modification of LDL by myeloperoxidase (MPO), a peroxidase enzyme secreted by leukocytes, has been established to promote vascular inflammation and cholesterol uptake by macrophages, a critical step in foam cell formation. In cell studies, we demonstrated that MPO modified TRL (MPO-TRL) exerted an adverse effect in human umbilical vein endothelial cells (HUVEC), as evidenced by an upregulation of mRNA expression of pro-inflammatory adhesion molecules. MPO-TRL co-incubation also resulted in a reduction in endothelial cell proliferation which can be restored by co-incubation with HDL. Cells treated with MPO-TRL also demonstrated an increase in expression of proteins involved in responses to hypoxia (HIF1ɑ) and in angiogenesis (VEGF) and a reduced expression of the cholesterol transporter ABCG1. We are further interested in whether triglyceride mediator ApoC-III exerts similar adverse effect in atherosclerosis in the settings of mouse models with dyslipidaemia and diabetes. We demonstrated that ApoC-III was present within plaque and the presence was positively associated with lesion size and inflammatory marker CD68. ApoC-III has been well characterised to induce endothelial cell inflammation, whether ApoC-III will induce inflammation in other vascular cells will be of additional interest in future studies. We have also found that using patients’ serum stratified with different levels of triglyceride, ApoC-III levels inversely correlated with HepG2 expression of both PPARɑ and cholesterol transporter ABCA1, important factors which involved in the synthesis of both ApoAI and HDL and subsequent effects on lipid transport. Further experiments are needed to demonstrate the correlation of ApoC-III in HDL metabolism in large, prospective cohorts. In summary, these observations described potential adverse effects of triglycerides and ApoC-III on vascular cells, atherosclerosis and lipid metabolism. The findings support potential causal effets and novel targets for therapeutic targeting to prevent atherosclerotic disease.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2020

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LIU, I. LIN, and 劉怡麟. "Association between hypertriglyceridemia and apolipoprotien C-III/lipoprotein lipase gene polymorphism in Taiwan Aborigines." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/77919163595950444735.

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碩士
高雄醫學大學
醫學研究所
91
Abstract Background － Hypertriglyceridemia(HTG) is a heterogeneous metabolic disorder. Effects of environmental factors and two genetic polymorphisms, an SstI polymorphism of Apolipoprotein C III gene and a Hind III polymorphism of lipoprotein lipase gene, on risk of HTG were analyzed in 250 Taiwan aborigines with or without HTG. Methods － This is a cross-sectional study of 250 southern Taiwan aborigines, which composed Paiwan tribe and Amis tribe, with 90 cases in the HTG group and 160 with normal serum triglycerides (NTG) recruited from community Health examinations. HTG is defined as > 150 mg/dl according to report by National Cholesterol Education Program (2001). Demographic data and dietary habits were collected by trained interviewers using structured questionaires. Polymerase chain reaction — restriction fragment length polymorphism (PCR — RFLP) was performed to define gene polymorphisms. Results － The respective SstI major allele (S1) and minor allele (S2) frequencies were 66.1﹪and 33.9﹪in HTG group and 73.6% and 26.4 % in NTG group (p<0.1). As analyzed exclusively in female subjects, frequencies of S2 allele was significantly higher (p<0.03) in HTG. The frequencies of the HindIII major allele (H+) and minor allele (H-) were similar between HTG (H+ 84.3﹪; H-:15.7﹪) and NTG (H+ 78.9%; H-:21.1%). Multiple logistic regression analysis reveals that Amis tribe, betel-chewing, starchy food, and plasma ApoC3concentrations were independently associated with risk of HTG. Furthermore, ApoC3 concentrations were increased (p<0.01) in a dose response manner among subjects with APOCIII s1s1, s1s2 and s2s2 genotypes accordingly. Conclusions－ In conclusion, our analyses suggest that molecular variants of APOC III(Sst І) polymorphism may be associated risk of HTG in Taiwan Aborigines.

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Perng, Tsae-Feng, and 彭彩鳳. "Effect of dietary fat and insulin on apolipoprotein C-II and apolipoprotein C-III gene expression in rats." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/46926500178605193115.

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碩士
靜宜大學
食品營養研究所
88
Hypertriglyceridemias are important risk factors for cardiovascular disease. Lipoprotein lipase (LPL, EC 3.1.1.34) plays an important role in lipid metabolism. The enzyme is activated by apolipoprotein C-II (ApoC-II) and inhibited by apolipoprotein C-III (ApoC-III). Because impaired LPL activity will lead to hypertriglyceridemia, therefore, the purpose of this research project was to study the effects of dietary fat and insulin on apoC-II and apoC-III gene expression. First, forty-eight male SD rats were divided into 6 groups and fed diets containing 7.5%, 15% and 30% of lard and soybean oil for 2 weeks, respectively. The concentrations of fasting total cholesterol (TC) and triglyceride (TG) in blood and the concentrations of apoC-II and apoC-III mRNA in liver and intestine were measured. After 2 weeks, fasting total cholesterol was not affected by the regimen, however, the concentrations of serum triglyceride in rats fed 30% soybean oil diet was significantly lower than those rats fed 7.5% and 15﹪soybean oil diet. Second, twenty-eight male Wistar rats were divided into 4 groups: control, diabetic group (streptozotocin-induced), insulin-treated for 1d group and insulin treated for 3d group. At the end of each period, the concentrations of serum glucose and triglyceride, and the concentrations of apoC-II and apoC-III mRNA in liver and intestine were measured. After treated with insulin, blood glucose and triglyceride levels were decreased significantly in diabetic rats, compared to their basal levels. However, both hepatic and intestinal apo C-II and apo C-III mRNA levels were not affected by insulin treatment. The results of this study suggest that intestinal apo C-II mRNA levels could be affected by the amount of dietary fat. It is possible that insulin is not a major hormonal factor, to regulate apo C-II and apo C-III gene expression in rats.

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Book chapters on the topic "Apolipoprotien C III"

1

Lackner, K. J., and D. Peetz. "Apolipoprotein C-III." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_270-1.

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Lackner, K. J., and D. Peetz. "Apolipoprotein C-III." In Springer Reference Medizin, 191. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_270.

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Humphries, Steve, Vilmundur Gudnason, Hiroko Paul-Hayase, N. Saha, and Maryvonne Rosseneu. "Identification of Common Genetic Polymorphisms that Determine Plasma Levels of ApoAI and HDL-C." In Human Apolipoprotein Mutants III, 247–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84634-2_22.

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4

Ordovas, Jose M., Dianne C. King, and Ernst J. Schaefer. "Familial Apolipoprotein A-I, C-III and A-IV Deficiency." In Human Apolipoprotein Mutants 2, 157–59. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-9549-6_19.

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Ferrell, R. E., M. I. Kamboh, B. S. Sepehrnia, L. L. Adams-Campbell, and K. M. Weiss. "Genetic Variation in the Apolipoproteins C-II and C-III." In Advances in Experimental Medicine and Biology, 81–85. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0733-4_11.

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Fruchart, J. C., V. Clavey, G. Luc, J. Dallongeville, B. Staels, and J. Auwerx. "Apolipoprotein C-III, An Important Player in Lipoprotein Metabolism." In Drugs Affecting Lipid Metabolism, 631–38. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_74.

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Norum, Robert A., Trudy M. Forte, Petar Alaupovic, and Henry N. Ginsberg. "Clinical Syndrome and Lipid Metabolism in Hereditary Deficiency of Apolipoproteins A-I and C-III, Variant 1." In Lipoprotein Deficiency Syndromes, 137–49. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1262-8_13.

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Kashyap, Moti L. "[12] Immunochemical methods for quantification of human apolipoprotein C-III." In Methods in Enzymology, 208–18. Elsevier, 1996. http://dx.doi.org/10.1016/s0076-6879(96)63014-6.

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Jackson, Richard L., and George Holdsworth. "[14] Isolation and properties of human apolipoproteins C-I, C-II, and C-III." In Methods in Enzymology, 288–97. Elsevier, 1986. http://dx.doi.org/10.1016/0076-6879(86)28074-x.

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Karathanasis, Sotirios K., Vassilis I. Zannis, and Jan L. Breslow. "[41] Characterization of the apolipoprotein A-I—C-III gene complex." In Methods in Enzymology, 712–26. Elsevier, 1986. http://dx.doi.org/10.1016/0076-6879(86)28101-x.

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