Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl

PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników
Czasopismo
2014 | 10 | 1 |
Tytuł artykułu

Postprandial decrease in LDL-cholesterol in men with metabolic syndrome

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Background: In some epidemiological studies, blood lipids are determined at non-fasting state, which may impact cardiovascular risk estimation. The aim of this study was to evaluate postprandial LDL-C changes in men with newly diagnosed metabolic syndrome (MetSy). Methods: 36 male patients were examined: 12 men with and 24 men without MetSy. The fat tolerance test was performed before and after a three-month hypolipidemic treatment. Serum lipids were measured using routine methods, lipid peroxides (LPO) colorimetrically, apoli- poproteins A-I, B, and hsCRP immunoturbidimetrically. Results: The postprandial increase in triglycerides was associated with a decrease in LDL-C and a small decrease in apo B. In men with MetSy, the mean change in LDL-C (-19.5 ± 2.3 mg/dl) was greater than in healthy men (-5.7 ± 3.8 mg/dl). All lipid changes (ΔTG, ΔLDL-C and ΔLPO) were linearly dependent on the postprandial non-LDL-choles- terol. After three months of hypolipidemic treatment, in all men with MetSy, the apoB/apoA-I ratio remained the same as before the therapy. Conclusion: In men diagnosed with MetSy, postprandial decreases in LDL-cholesterol may cause underestimation of cardiovascular risk. After three months of hypolipidemic treatment, there was only a partial reduction in this risk, as the apoB/apoA-I ratio remained the same.
Wydawca

Czasopismo
Rocznik
Tom
10
Numer
1
Opis fizyczny
Daty
otrzymano
2013-10-20
zaakceptowano
2014-03-31
online
2015-02-03
Twórcy
  • Wroclaw Medical University, Department of Internal and Occupational Diseases, and Hypertension, Borowska 213, 50-556 Wrocław, Poland
  • Department of Internal Diseases and Hypertension, Wroclaw Medical University, Wrocław, Poland
  • Department of Internal Diseases and Hypertension, Wroclaw Medical University, Wrocław, Poland
  • Department of Internal Diseases and Hypertension, Wroclaw Medical University, Wrocław, Poland
  • Department of Internal Diseases and Hypertension, Wroclaw Medical University, Wrocław, Poland
  • Department of Internal Diseases and Hypertension, Wroclaw Medical University, Wrocław, Poland
Bibliografia
  • [1] Reaven GM. The Metabolic Syndrome: Requiescat in Pace. ClinChem. 2005; 51: 931-938[Crossref]
  • [2] Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI,Donato KA, et al. Harmonizing the metabolic syndrome: a jointinterim statement of the International Diabetes FederationTask Force on Epidemiology and Prevention; National Heart,Lung, and Blood Institute; American Heart Association; WorldHeart Federation; International Atherosclerosis Society; andInternational Association for the Study of Obesity. Circulation.2009;120:1640–1645
  • [3] Achimastos AD, Efstathiou SP, Christoforatos T, Panagiotou TN,Stergiou GS, Mountokalakis TD. Arterial stiffness: determinantsrelationship to the metabolic syndrome. Angiology.2007;58:11-20[WoS][Crossref]
  • [4] Beijers HJ, Henry RM, Bravenboer B, Ferreira I, Dekker JM,Nijpels G, Stehouwer CD.Metabolic Syndrome in NondiabeticIndividuals Associated With Maladaptive Carotid Remodeling:The Hoorn Study.Am J Hypertens. 2011 Jan 6. [Crossref]
  • [Epub ahead ofprint].[PubMed]
  • [5] Tzou WS, Douglas PS, Srinivasan SR, Chen W, Berenson G,Stein JH. Advanced lipoprotein testing does not improve identificationof subclinical atherosclerosis in young adults: theBogalusa Heart Study. ANN Intern Med. 2005;142:742-50
  • [6] Galassi A, Reynolds K, He J. Metabolic syndrome and riskof cardiovascular disease: a meta-analysis. Am J Med.2006;119:812–819[Crossref]
  • [7] Gami AS, Witt BJ, Howard DE, Erwin PJ, Gami LA, SomersVK, Montori VM. Metabolic syndrome and risk of incidentcardiovascular events and death: a systematic review andmeta-analysis of longitudinal studies. J Am Coll Cardiol.2007;49:403–414[WoS][Crossref]
  • [8] Mottillo S, Filion KB, Genest J, Joseph L, Pilote L, PoirierP, Rinfret S, Schiffrin EL, Eisenberg MJ. The metabolicsyndrome and cardiovascular risk. A systematic review andmeta-analysis. J Am CollCardiol. 2010;56:1113–1132[Crossref]
  • [9] Li J, Flammer AJ, Lennon RJ, Nelson RE, Gulati R, FriedmanPA, Thomas RJ, Sandhu NP, Hua Q, Lerman LO, Lerman A.Comparison of the effect of the metabolic syndrome andmultiple traditional cardiovascular risk factors on vascularfunction. Mayo Clin Proc. 2012;87:968-75[WoS][Crossref]
  • [10] Nofer JR, Kehre B, Fobker M, Levkau B, Assman G, vonEckardstein A. HDL and arteriosclerosis: beyond reversecholesterol transport. Atherosclerosis. 2002;161:1-16.
  • [11] Barter P. The role of HDL-cholesterol in preventing atheroscleroticdisease. Eur Heart J Suppl 2005;7:F4-F8[Crossref]
  • [12] Andrews KL, Moore XL, Chin-Dusting JP. Anti-atherogeniceffects of high-density lipoprotein on nitric oxide synthesis inthe endothelium.Clin Exp Pharmacol Physiol. 2010;37:736-42[Crossref][WoS]
  • [13] Onat A, Can G, Yüksel H. Dysfunction of high-densitylipoprotein and its apolipoproteins: New mechanismsunderlying cardiometabolic risk in the population at large TurkKardiyol Dern Ars. 2012;40:368-85
  • [14] Calabro P, Yeh ETH. Intra-abdominal adiposity, inflammation,and cardiovascular risk: New insight into global cardiometabolicrisk.Current Hypertension Rep. 2008;10:32-38
  • [15] Yuan G, Al-Shali KZ, Hegele R. Hypertriglyceridemia: itsetiology, effects and treatment. CMAJ. 2007;176:1113-1120
  • [16] Hansel B, Giral P, Nobecourt E, et al. Metabolic syndrome isassociated with elevated oxidative stress and dysfunctionaldense high-density lipoprotein particles displayingimpaired antioxidative activity. J Clin Endocrinol Metab.2004;89:4963-4971[Crossref]
  • [17] Bai H, Liu BW, Deng ZY, Shen T, Fang DZ, Zhao YH, Liu Y. Plasmavery-low-density lipoprotein, low-density lipoprotein, andhigh-density lipoprotein oxidative modification inducesprocoagulant profiles in endogenous hypertriglyceridemia.Free Radic Biol Med. 2006;40:1796-803
  • [18] Kolovou GD, Mikhailidis DP, Kovar J, Lairon D, NordestgaardBG, Ooi TC, Perez-Martinez P, Bilianou H, AnagnostopoulouK, Panotopoulos G. Assessment and clinical relevance ofnon-fasting and postprandial triglycerides: an expert panelstatement. Curr Vasc Pharmacol. 2011;9:258-270[Crossref]
  • [19] Nordestgaard BG, Freiberg JJ. Clinical relevance of non-fastingand postprandial hypertriglyceridemia and remnantcholesterol.CurrVascPharmacol. 2011;9:281-6
  • [20] Salazar MR, Carbajal HA, Espeche WG, LeivaSisnieguez CE,Balbín E, Dulbecco CA, Aizpurúa M, Marillet AG, ReavenGM. Relation among the plasma triglyceride/high-densitylipoprotein cholesterol concentration ratio, insulin resistance,and associated cardio-metabolic risk factors in men andwomen. Am J Cardiol. 2012;109:1749-53[Crossref][WoS]
  • [21] Grundy SM; National Cholesterol Education Program (NCEP)-TheNational Cholesterol Guidelines in 2001, Adult Treatment Panel(ATP) III. Approach to lipoprotein management in 2001 NationalCholesterol Guidelines. Am J Cardiol. 2002; 90:11i-21i
  • [22] Fruchart JC, Duriez P. Mode of action of fibrates in theregulation of triglyceride and HDL-cholesterol metabolism.Drugs Today. 2006;42:39-64.
  • [23] Stone NJ, Saxon D. Approach to treatment of the patientwith metabolic syndrome: lifestyle therapy.Am J Cardiol.2005;96:15E-21E[Crossref]
  • [24] Goodson BL, Wung SF, Archbold KH. Obstructive sleepapnea hypopnea syndrome and metabolic syndrome: Asynergistic cardiovascular risk factor. J Am Acad Nurse Pract.2012;24:695-703[WoS][Crossref]
  • [25] Walldius G, Aastveit AH, Jungner I. Stroke mortality and theapoB/apoA-I ratio: results of the AMORIS prospective study. JIntern Med. 2006;259:259-66[Crossref]
  • [26] Jungner I, Sniderman AD, Furberg C, Aastveit AH, HolmeI, Walldius G. Does low-density lipoprotein size add toatherogenic particle number in predicting the risk of fatalmyocardial infarction? Am J Cardiol. 2006;97:943-6[Crossref]
  • [27] Contois JH, Warnick GR, Sniderman AD. Reliability oflow-density lipoprotein cholesterol, non-high-densitylipoprotein cholesterol, and apolipoprotein B measurement. JClin Lipidol. 2011;5:264-72[Crossref][WoS]
  • [28] Walldius G. Apolipoprotein B (apoB) more closely related tosubclinical atherosclerosis than non-HDL cholesterol and LDLcholesterol. J Intern Med. 2010;268:549-51[WoS]
  • [29] Sniderman AD, Williams K, Contois JH, Monroe HM, McQueenMJ, de Graaf J, Furberg CD. A meta-analysis of low-densitylipoprotein cholesterol, non-high-density lipoproteincholesterol, and apolipoprotein B as markers of cardiovascularrisk.CircCardiovascQual Outcomes. 2011;4:337-452
  • [30] Sundvall J, Leiviskä J, Laatikainen T, Peltonen M, Salomaa V,Vanhala M, Korpi-Hyövälti E, Lauronen J, Alfthan G. The use offasting vs. non-fasting triglyceride concentration for estimating the prevalence of high LDL-cholesterol and metabolicsyndromein population surveys. BMC Med Res Methodol. 2011;11:63[Crossref]
  • [31] Lund SS, Petersen M, Frandsen M, Smidt UM, Parving HH,Vaag AA, Jensen T.Agreement between fasting and postprandialLDLcholesterolmeasuredwith 3methods in patients withtype2diabetesmellitus. Clin Chem. 2011;57:298-308
  • [32] Liskum L. Cholesterol biosynthesis. New ComprehensiveBiochemistry. 2002;36: 409-432
  • [33] Ruge T, Sukonina V, Kroupa O, Makoveichuk E, Lundgren M,Svensson MK, Olivecrona G, Eriksson JW. Effects of hyperinsulinemiaon lipoprotein lipase, angiopoietin-like protein4, and glycosylphosphatidylinositol-anchored high-densitylipoprotein binding protein 1 in subjects with and without type2 diabetes mellitus. Metabolism. 2012;61:652-60[Crossref]
  • [34] Zélie J, Fournier N, Bellanger N, Chapman MJ, Goff WL, GuerinM. Postprandial lipemiaenhances the capacity of largeHDL2 particles to mediate free cholesterol efflux via SR-BIand ABCG1 pathways in type IIB hyperlipidemia. J Lipid Res.2010;51:3350-3358
  • [35] Isomaa B, Almgren P, Tuomi T, Forsén B, Lahti K, NissénM, Taskinen MR. Cardiovascular Morbidity and MortalityAssociated With the Metabolic Syndrome. Diabetes Care. 2001;24:683–689.[Crossref]
  • [36] Virani SS, Wang D, Woodard LD, Chitwod SS, Landrum CR, ZieveFJ, Ballantyne CM, Petersen LA. Non–high-density lipoproteincholesterol reporting and goal attainment in primary care. J ClinLipidol. 2012;6:545-552[Crossref][WoS]
  • [37] Stancliffe RA, Thorpe T, Zemel MB. Dairy attentuates oxidativeand inflammatory stress in metabolic syndrome. Am J ClinNutr.2011;94:422-430
  • [38] Pravenec M, Kajiya T, Zídek V, Landa V, Mlejnek P, Simáková M,Silhavý J, Malínská H, Oliyarnyk O, Kazdová L, Fan J, Wang J,Kurtz TW. Effects of human C-reactive protein on pathogenesisof features of the metabolic syndrome. Hypertension.2011;57:731-737[WoS][Crossref]
  • [39] Mazloom Z, Hejazi N, Dabbaghmanesh MH, Tabatabaei HR,Ahmadi A, Ansar H. Effect of vitamin C supplementationon postprandial oxidative stress and lipid profile in type 2diabeticpatients. Pak J Biol Sci. 2011;14:900-904
  • [40] Spiteller G.The relation of lipid peroxidation processes withatherogenesis: a new theory on atherogenesis. Mol Nutr FoodRes. 2005;49:999-1013[Crossref]
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_1515_med-2015-0025
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.