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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/47097完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張國柱(Kuo-Chu Chang) | |
| dc.contributor.author | Ya-Wan Huang | en |
| dc.contributor.author | 黃雅琬 | zh_TW |
| dc.date.accessioned | 2021-06-15T05:47:29Z | - |
| dc.date.available | 2013-01-12 | |
| dc.date.copyright | 2011-10-05 | |
| dc.date.issued | 2011 | |
| dc.date.submitted | 2011-08-19 | |
| dc.identifier.citation | 參考文獻
Akbiyik F, Ray DM, Bozkaya H, Demirpence E (2004). Ligand- and species-dependent activation of PPARalpha. Cell Physiol Biochem 14(4-6): 269-276. Ammerschlaeger M, Beigel J, Klein KU, Mueller SO (2004). Characterization of the species-specificity of peroxisome proliferators in rat and human hepatocytes. Toxicol Sci 78(2): 229-240. An D, Rodrigues B (2006). Role of changes in cardiac metabolism in development of diabetic cardiomyopathy. Am J Physiol Heart Circ Physiol 291(4): H1489-1506. Arora MK, Reddy K, Balakumar P (2010). The low dose combination of fenofibrate and rosiglitazone halts the progression of diabetes-induced experimental nephropathy. Eur J Pharmacol 636(1-3): 137-144. Balakumar P, Rohilla A, Mahadevan N (2011). Pleiotropic actions of fenofibrate on the heart. Pharmacol Res 63(1): 8-12. Barbier O, Torra IP, Duguay Y, Blanquart C, Fruchart JC, Glineur C, et al. (2002). Pleiotropic actions of peroxisome proliferator-activated receptors in lipid metabolism and atherosclerosis. Arterioscler Thromb Vasc Biol 22(5): 717-726. Beckman JA, Creager MA, Libby P (2002). Diabetes and atherosclerosis: epidemiology, pathophysiology, and management. JAMA 287(19): 2570-2581. Braissant O, Foufelle F, Scotto C, Dauca M, Wahli W (1996). Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat. Endocrinology 137(1): 354-366. Brandt JM, Djouadi F, Kelly DP (1998). Fatty acids activate transcription of the muscle carnitine palmitoyltransferase I gene in cardiac myocytes via the peroxisome proliferator-activated receptor alpha. J Biol Chem 273(37): 23786-23792. Brownlee M (2005). The pathobiology of diabetic complications: a unifying mechanism. Diabetes 54(6): 1615-1625. Bulhak AA, Jung C, Ostenson CG, Lundberg JO, Sjoquist PO, Pernow J (2009). PPAR-alpha activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway. Am J Physiol Heart Circ Physiol 296(3): H719-727. Burattini R, Fioretti S, Jetto L (1985). A simple algorithm for defining the mean cardiac cycle of aortic flow and pressure during steady state. Comput Biomed Res 18(4): 303-312. Carmena R (2005). Type 2 diabetes, dyslipidemia, and vascular risk: rationale and evidence for correcting the lipid imbalance. Am Heart J 150(5): 859-870. Caslake MJ, Packard CJ, Gaw A, Murray E, Griffin BA, Vallance BD, et al. (1993). Fenofibrate and LDL metabolic heterogeneity in hypercholesterolemia. Arterioscler Thromb 13(5): 702-711. Cattin L, Da Col PG, Feruglio FS, Finazzo L, Rimondi S, Descovich G, et al. (1990). Efficacy of ciprofibrate in primary type II and IV hyperlipidemia: the Italian multicenter study. Clin Ther 12(6): 482-488. Chang KC, Hsu KL, Tseng YZ (2003). Effects of diabetes and gender on mechanical properties of the arterial system in rats: aortic impedance analysis. Exp Biol Med (Maywood) 228(1): 70-78. Chang KC, Liang JT, Tsai PS, Wu MS, Hsu KL (2009). Prevention of arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen. Br J Pharmacol 157(8): 1419-1426. Chang KC, Tseng CD, Chou TF, Cho YL, Chi TC, Su MJ, et al. (2006). Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes. Eur J Clin Invest 36(1): 1-7. Chang KC, Tseng CD, Lu SC, Liang JT, Wu MS, Tsai MS, et al. (2010). Effects of acetyl-L-carnitine and oxfenicine on aorta stiffness in diabetic rats. Eur J Clin Invest 40(11): 1002-1010. Chang KS, Lund DD (1986). Alterations in the baroreceptor reflex control of heart rate in streptozotocin diabetic rats. J Mol Cell Cardiol 18(6): 617-624. Chen YJ, Quilley J (2008). Fenofibrate treatment of diabetic rats reduces nitrosative stress, renal cyclooxygenase-2 expression, and enhanced renal prostaglandin release. J Pharmacol Exp Ther 324(2): 658-663. Chew GT, Watts GF, Davis TM, Stuckey BG, Beilin LJ, Thompson PL, et al. (2008). Hemodynamic effects of fenofibrate and coenzyme Q10 in type 2 diabetic subjects with left ventricular diastolic dysfunction. Diabetes Care 31(8): 1502-1509. Chinetti G, Gbaguidi FG, Griglio S, Mallat Z, Antonucci M, Poulain P, et al. (2000). CLA-1/SR-BI is expressed in atherosclerotic lesion macrophages and regulated by activators of peroxisome proliferator-activated receptors. Circulation 101(20): 2411-2417. Chinetti G, Lestavel S, Bocher V, Remaley AT, Neve B, Torra IP, et al. (2001). PPAR-alpha and PPAR-gamma activators induce cholesterol removal from human macrophage foam cells through stimulation of the ABCA1 pathway. Nat Med 7(1): 53-58. Daneman D (2006). Type 1 diabetes. Lancet 367(9513): 847-858. De Vriese AS, Verbeuren TJ, Van de Voorde J, Lameire NH, Vanhoutte PM (2000). Endothelial dysfunction in diabetes. Br J Pharmacol 130(5): 963-974. Delerive P, De Bosscher K, Besnard S, Vanden Berghe W, Peters JM, Gonzalez FJ, et al. (1999a). Peroxisome proliferator-activated receptor alpha negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-kappaB and AP-1. J Biol Chem 274(45): 32048-32054. Delerive P, Martin-Nizard F, Chinetti G, Trottein F, Fruchart JC, Najib J, et al. (1999b). Peroxisome proliferator-activated receptor activators inhibit thrombin-induced endothelin-1 production in human vascular endothelial cells by inhibiting the activator protein-1 signaling pathway. Circ Res 85(5): 394-402. Desvergne B, Wahli W (1999). Peroxisome proliferator-activated receptors: nuclear control of metabolism. Endocr Rev 20(5): 649-688. Devchand PR, Keller H, Peters JM, Vazquez M, Gonzalez FJ, Wahli W (1996). The PPARalpha-leukotriene B4 pathway to inflammation control. Nature 384(6604): 39-43. Dillmann WH (1980). Diabetes mellitus induces changes in cardiac myosin of the rat. Diabetes 29(7): 579-582. Dincer UD, Bidasee KR, Guner S, Tay A, Ozcelikay AT, Altan VM (2001). The effect of diabetes on expression of beta1-, beta2-, and beta3-adrenoreceptors in rat hearts. Diabetes 50(2): 455-461. Drukala J, Urbanska K, Wilk A, Grabacka M, Wybieralska E, Del Valle L, et al. (2010). ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro. Mol Cancer 9: 159. Duncan JG, Finck BN (2008). The PPARalpha-PGC-1alpha Axis Controls Cardiac Energy Metabolism in Healthy and Diseased Myocardium. PPAR Res 2008: 253817. Evans RM, Barish GD, Wang YX (2004). PPARs and the complex journey to obesity. Nat Med 10(4): 355-361. Finck BN, Han X, Courtois M, Aimond F, Nerbonne JM, Kovacs A, et al. (2003). A critical role for PPARalpha-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy: modulation by dietary fat content. Proc Natl Acad Sci U S A 100(3): 1226-1231. Finck BN, Lehman JJ, Leone TC, Welch MJ, Bennett MJ, Kovacs A, et al. (2002). The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus. J Clin Invest 109(1): 121-130. Forcheron F, Abdallah P, Basset A, del Carmine P, Haffar G, Beylot M (2009). Nonalcoholic hepatic steatosis in Zucker diabetic rats: spontaneous evolution and effects of metformin and fenofibrate. Obesity (Silver Spring) 17(7): 1381-1389. Forman BM, Chen J, Evans RM (1997). Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta. Proc Natl Acad Sci U S A 94(9): 4312-4317. Fruchart JC, Duriez P, Staels B (1999). [Molecular mechanism of action of the fibrates]. J Soc Biol 193(1): 67-75. Fruchart JC, Staels B, Duriez P (2001). PPARS, metabolic disease and atherosclerosis. Pharmacol Res 44(5): 345-352. Furchgott RF, Vanhoutte PM (1989). Endothelium-derived relaxing and contracting factors. FASEB J 3(9): 2007-2018. Gando S, Hattori Y, Akaishi Y, Nishihira J, Kanno M (1997). Impaired contractile response to beta adrenoceptor stimulation in diabetic rat hearts: alterations in beta adrenoceptors-G protein-adenylate cyclase system and phospholamban phosphorylation. J Pharmacol Exp Ther 282(1): 475-484. George C, Lochner A, Huisamen B (2011). The efficacy of Prosopis glandulosa as antidiabetic treatment in rat models of diabetes and insulin resistance. J Ethnopharmacol. Gertz EW, Wisneski JA, Stanley WC, Neese RA (1988). Myocardial substrate utilization during exercise in humans. Dual carbon-labeled carbohydrate isotope experiments. J Clin Invest 82(6): 2017-2025. Goldbourt U, Yaari S, Medalie JH (1997). Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality. A 21-year follow-up of 8000 men. Arterioscler Thromb Vasc Biol 17(1): 107-113. Gonzalez FJ, Shah YM (2008). PPARalpha: mechanism of species differences and hepatocarcinogenesis of peroxisome proliferators. Toxicology 246(1): 2-8. Gordon DJ, Rifkind BM (1989). High-density lipoprotein--the clinical implications of recent studies. N Engl J Med 321(19): 1311-1316. Guo Q, Wang G, Namura S (2010). Fenofibrate improves cerebral blood flow after middle cerebral artery occlusion in mice. J Cereb Blood Flow Metab 30(1): 70-78. Hansen MK, McVey MJ, White RF, Legos JJ, Brusq JM, Grillot DA, et al. (2010). Selective CETP inhibition and PPARalpha agonism increase HDL cholesterol and reduce LDL cholesterol in human ApoB100/human CETP transgenic mice. J Cardiovasc Pharmacol Ther 15(2): 196-202. Heller F, Harvengt C (1983). Effects of clofibrate, bezafibrate, fenofibrate and probucol on plasma lipolytic enzymes in normolipaemic subjects. Eur J Clin Pharmacol 25(1): 57-63. Heyliger CE, Pierce GN, Singal PK, Beamish RE, Dhalla NS (1982). Cardiac alpha- and beta-adrenergic receptor alterations in diabetic cardiomyopathy. Basic Res Cardiol 77(6): 610-618. Hicks KK, Seifen E, Stimers JR, Kennedy RH (1998). Effects of streptozotocin-induced diabetes on heart rate, blood pressure and cardiac autonomic nervous control. J Auton Nerv Syst 69(1): 21-30. Huang J, Lin SC, Nadershahi A, Watts SW, Sarkar R (2008). Role of redox signaling and poly (adenosine diphosphate-ribose) polymerase activation in vascular smooth muscle cell growth inhibition by nitric oxide and peroxynitrite. J Vasc Surg 47(3): 599-607. Inaba T, Yagyu H, Itabashi N, Tazoe F, Fujita N, Nagashima S, et al. (2008). Cholesterol reduction and atherosclerosis inhibition by bezafibrate in low-density lipoprotein receptor knockout mice. Hypertens Res 31(5): 999-1005. Inoue I, Shino K, Noji S, Awata T, Katayama S (1998). Expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) in primary cultures of human vascular endothelial cells. Biochem Biophys Res Commun 246(2): 370-374. Irukayama-Tomobe Y, Miyauchi T, Sakai S, Kasuya Y, Ogata T, Takanashi M, et al. (2004). Endothelin-1-induced cardiac hypertrophy is inhibited by activation of peroxisome proliferator-activated receptor-alpha partly via blockade of c-Jun NH2-terminal kinase pathway. Circulation 109(7): 904-910. Issemann I, Green S (1990). Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators. Nature 347(6294): 645-650. Jonkers IJ, de Man FH, van der Laarse A, Frolich M, Gevers Leuven JA, Kamper AM, et al. (2001). Bezafibrate reduces heart rate and blood pressure in patients with hypertriglyceridemia. J Hypertens 19(4): 749-755. Kashiwagi A, Nishio Y, Saeki Y, Kida Y, Kodama M, Shigeta Y (1989). Plasma membrane-specific deficiency in cardiac beta-adrenergic receptor in streptozocin-diabetic rats. Am J Physiol 257(2 Pt 1): E127-132. Keech A, Simes RJ, Barter P, Best J, Scott R, Taskinen MR, et al. (2005). Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 366(9500): 1849-1861. Keller H, Dreyer C, Medin J, Mahfoudi A, Ozato K, Wahli W (1993). Fatty acids and retinoids control lipid metabolism through activation of peroxisome proliferator-activated receptor-retinoid X receptor heterodimers. Proc Natl Acad Sci U S A 90(6): 2160-2164. Kersten S, Desvergne B, Wahli W (2000). Roles of PPARs in health and disease. Nature 405(6785): 421-424. King GL, Shiba T, Oliver J, Inoguchi T, Bursell SE (1994). Cellular and molecular abnormalities in the vascular endothelium of diabetes mellitus. Annu Rev Med 45: 179-188. Koh EH, Kim MS, Park JY, Kim HS, Youn JY, Park HS, et al. (2003). Peroxisome proliferator-activated receptor (PPAR)-alpha activation prevents diabetes in OLETF rats: comparison with PPAR-gamma activation. Diabetes 52(9): 2331-2337. Larsen PJ, Jensen PB, Sorensen RV, Larsen LK, Vrang N, Wulff EM, et al. (2003). Differential influences of peroxisome proliferator-activated receptors gamma and -alpha on food intake and energy homeostasis. Diabetes 52(9): 2249-2259. Laxminarayan S, Sipkema P, Westerhof N (1978). Characterization of the arterial system in the time domain. IEEE Trans Biomed Eng 25(2): 177-184. Lee H, Shi W, Tontonoz P, Wang S, Subbanagounder G, Hedrick CC, et al. (2000). Role for peroxisome proliferator-activated receptor alpha in oxidized phospholipid-induced synthesis of monocyte chemotactic protein-1 and interleukin-8 by endothelial cells. Circ Res 87(6): 516-521. Lee JM, Choudhury RP (2010). Atherosclerosis regression and high-density lipoproteins. Expert Rev Cardiovasc Ther 8(9): 1325-1334. Lishner M, Akselrod S, Avi VM, Oz O, Divon M, Ravid M (1987). Spectral analysis of heart rate fluctuations. A non-invasive, sensitive method for the early diagnosis of autonomic neuropathy in diabetes mellitus. J Auton Nerv Syst 19(2): 119-125. Liu Z, Brin KP, Yin FC (1986). Estimation of total arterial compliance: an improved method and evaluation of current methods. Am J Physiol 251(3 Pt 2): H588-600. Lloyd-Mostyn RH, Watkins PJ (1975). Defective innervation of heart in diabetic autonomic neuropathy. Br Med J 3(5974): 15-17. Lopaschuk GD, Katz S, McNeill JH (1983). The effect of alloxan- and streptozotocin-induced diabetes on calcium transport in rat cardiac sarcoplasmic reticulum. The possible involvement of long chain acylcarnitines. Can J Physiol Pharmacol 61(5): 439-448. Louet JF, Chatelain F, Decaux JF, Park EA, Kohl C, Pineau T, et al. (2001). Long-chain fatty acids regulate liver carnitine palmitoyltransferase I gene (L-CPT I) expression through a peroxisome-proliferator-activated receptor alpha (PPARalpha)-independent pathway. Biochem J 354(Pt 1): 189-197. Lu K, Lee MH, Patel SB (2001). Dietary cholesterol absorption; more than just bile. Trends Endocrinol Metab 12(7): 314-320. Mandard S, Muller M, Kersten S (2004). Peroxisome proliferator-activated receptor alpha target genes. Cell Mol Life Sci 61(4): 393-416. Marx N, Sukhova GK, Collins T, Libby P, Plutzky J (1999). PPARalpha activators inhibit cytokine-induced vascular cell adhesion molecule-1 expression in human endothelial cells. Circulation 99(24): 3125-3131. Mascaro C, Acosta E, Ortiz JA, Marrero PF, Hegardt FG, Haro D (1998). Control of human muscle-type carnitine palmitoyltransferase I gene transcription by peroxisome proliferator-activated receptor. J Biol Chem 273(15): 8560-8563. Milnor WR (1975). Arterial impedance as ventricular afterload. Circ Res 36(5): 565-570. Mitchell GF, Pfeffer MA, Westerhof N, Pfeffer JM (1994). Measurement of aortic input impedance in rats. Am J Physiol 267(5 Pt 2): H1907-1915. Mudd JO, Borlaug BA, Johnston PV, Kral BG, Rouf R, Blumenthal RS, et al. (2007). Beyond low-density lipoprotein cholesterol: defining the role of low-density lipoprotein heterogeneity in coronary artery disease. J Am Coll Cardiol 50(18): 1735-1741. Mukherjee R, Jow L, Noonan D, McDonnell DP (1994). Human and rat peroxisome proliferator activated receptors (PPARs) demonstrate similar tissue distribution but different responsiveness to PPAR activators. J Steroid Biochem Mol Biol 51(3-4): 157-166. Neely JR, Rovetto MJ, Oram JF (1972). Myocardial utilization of carbohydrate and lipids. Prog Cardiovasc Dis 15(3): 289-329. Nichols WW, Conti CR, Walker WE, Milnor WR (1977). Input impedance of the systemic circulation in man. Circ Res 40(5): 451-458. Nichols WW, O'Rourke MF (2005). McDonald's Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. Nichols WW, Pepine CJ, Geiser EA, Conti CR (1980). Vascular load defined by the aortic input impedance spectrum. Fed Proc 39(2): 196-201. Noble M, Gade I, Frenchard D (1976). Blood pressure and flow in the ascending aorta of conscious dogs. Cardiovasc Res 1: 9-21. Oyama Y, Kawasaki H, Hattori Y, Kanno M (1986). Attenuation of endothelium-dependent relaxation in aorta from diabetic rats. Eur J Pharmacol 132(1): 75-78. Pabbidi RM, Cao DS, Parihar A, Pauza ME, Premkumar LS (2008). Direct role of streptozotocin in inducing thermal hyperalgesia by enhanced expression of transient receptor potential vanilloid 1 in sensory neurons. Mol Pharmacol 73(3): 995-1004. Panagia M, Gibbons GF, Radda GK, Clarke K (2005). PPAR-alpha activation required for decreased glucose uptake and increased susceptibility to injury during ischemia. Am J Physiol Heart Circ Physiol 288(6): H2677-2683. Pandolfi A, De Filippis EA (2007). Chronic hyperglicemia and nitric oxide bioavailability play a pivotal role in pro-atherogenic vascular modifications. Genes Nutr 2(2): 195-208. Park CW, Zhang Y, Zhang X, Wu J, Chen L, Cha DR, et al. (2006). PPARalpha agonist fenofibrate improves diabetic nephropathy in db/db mice. Kidney Int 69(9): 1511-1517. Pasceri V, Cheng JS, Willerson JT, Yeh ET (2001). Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation 103(21): 2531-2534. Patel KP, Zhang PL (1989). Reduced renal responses to volume expansion in streptozotocin-induced diabetic rats. Am J Physiol 257(3 Pt 2): R672-679. Patel KP, Zhang PL, Zeigler DW, Kauker ML (1997). Renal response to volume expansion in streptozotocin-induced diabetic rats: influence of calcium channel blockade. Diabetes Res Clin Pract 35(2-3): 69-74. Pekkanen J, Linn S, Heiss G, Suchindran CM, Leon A, Rifkind BM, et al. (1990). Ten-year mortality from cardiovascular disease in relation to cholesterol level among men with and without preexisting cardiovascular disease. N Engl J Med 322(24): 1700-1707. Peng YI, Chang KC (2000). Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis. Can J Physiol Pharmacol 78(5): 415-422. Pepine CJ, Nichols WW (1982). Aortic input impedance in cardiovascular disease. Prog Cardiovasc Dis 24(4): 307-318. Qu S, Su D, Altomonte J, Kamagate A, He J, Perdomo G, et al. (2007). PPAR{alpha} mediates the hypolipidemic action of fibrates by antagonizing FoxO1. Am J Physiol Endocrinol Metab 292(2): E421-434. Ramanadham S, McNeill JH, Tenner TE, Jr. (1986). Experimentally induced effects of diabetes on the rat myocardial beta-adrenoceptor system. Proc West Pharmacol Soc 29: 23-25. Robinson E, Grieve DJ (2009). Significance of peroxisome proliferator-activated receptors in the cardiovascular system in health and disease. Pharmacol Ther 122(3): 246-263. Ross J, Covell J, Sonnenbuck E, Braunwald E (1996). Contractile state of the heart characterized by force-velocity relations in variable afterload and isovolumic beats. Cardiovasc Res 18: 149-163. Ross R (1993). The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362(6423): 801-809. Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, Elam MB, et al. (1999). Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med 341(6): 410-418. Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, et al. (1996). The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med 335(14): 1001-1009. Saddik M, Lopaschuk GD (1991). Myocardial triglyceride turnover and contribution to energy substrate utilization in isolated working rat hearts. J Biol Chem 266(13): 8162-8170. Saito K, Kuroda A, Tanaka H (1991). Characterisation of beta 1 and beta 2 adrenoceptor subtypes in the atrioventricular node of diabetic rat hearts by quantitative autoradiography. Cardiovasc Res 25(11): 950-954. Schoonjans K, Martin G, Staels B, Auwerx J (1997). Peroxisome proliferator-activated receptors, orphans with ligands and functions. Curr Opin Lipidol 8(3): 159-166. Schoonjans K, Staels B, Auwerx J (1996). The peroxisome proliferator activated receptors (PPARS) and their effects on lipid metabolism and adipocyte differentiation. Biochim Biophys Acta 1302(2): 93-109. Schwartz CJ, Valente AJ, Sprague EA, Kelley JL, Cayatte AJ, Rozek MM (1992). Pathogenesis of the atherosclerotic lesion. Implications for diabetes mellitus. Diabetes Care 15(9): 1156-1167. Shaw JE, Zimmet PZ, McCarty D, de Courten M (2000). Type 2 diabetes worldwide according to the new classification and criteria. Diabetes Care 23 Suppl 2: B5-10. Slatter DA, Bolton CH, Bailey AJ (2000). The importance of lipid-derived malondialdehyde in diabetes mellitus. Diabetologia 43(5): 550-557. Slatter DA, Paul RG, Murray M, Bailey AJ (1999). Reactions of lipid-derived malondialdehyde with collagen. J Biol Chem 274(28): 19661-19669. Smith JM, Paulson DJ, Romano FD (1997). Inhibition of nitric oxide synthase by L-NAME improves ventricular performance in streptozotocin-diabetic rats. J Mol Cell Cardiol 29(9): 2393-2402. Stadler K, Jenei V, Somogyi A, Jakus J (2005). Beneficial effects of aminoguanidine on the cardiovascular system of diabetic rats. Diabetes Metab Res Rev 21(2): 189-196. Staels B, Koenig W, Habib A, Merval R, Lebret M, Torra IP, et al. (1998). Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators. Nature 393(6687): 790-793. Staels B, Vu-Dac N, Kosykh VA, Saladin R, Fruchart JC, Dallongeville J, et al. (1995). Fibrates downregulate apolipoprotein C-III expression independent of induction of peroxisomal acyl coenzyme A oxidase. A potential mechanism for the hypolipidemic action of fibrates. J Clin Invest 95(2): 705-712. Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL (1989). Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med 320(14): 915-924. Sundaresan PR, Sharma VK, Gingold SI, Banerjee SP (1984). Decreased beta-adrenergic receptors in rat heart in streptozotocin-induced diabetes: role of thyroid hormones. Endocrinology 114(4): 1358-1363. Tabernero A, Schoonjans K, Jesel L, Carpusca I, Auwerx J, Andriantsitohaina R (2002). Activation of the peroxisome proliferator-activated receptor alpha protects against myocardial ischaemic injury and improves endothelial vasodilatation. BMC Pharmacol 2: 10. Tordjman K, Bernal-Mizrachi C, Zemany L, Weng S, Feng C, Zhang F, et al. (2001). PPARalpha deficiency reduces insulin resistance and atherosclerosis in apoE-null mice. J Clin Invest 107(8): 1025-1034. Tordjman KM, Semenkovich CF, Coleman T, Yudovich R, Bak S, Osher E, et al. (2007). Absence of peroxisome proliferator-activated receptor-alpha abolishes hypertension and attenuates atherosclerosis in the Tsukuba hypertensive mouse. Hypertension 50(5): 945-951. Vavra JJ, Deboer C, Dietz A, Hanka LJ, Sokolski WT (1959). Streptozotocin, a new antibacterial antibiotic. Antibiot Annu 7: 230-235. Violi F, Marino R, Milite MT, Loffredo L (1999). Nitric oxide and its role in lipid peroxidation. Diabetes Metab Res Rev 15(4): 283-288. Wayman NS, Hattori Y, McDonald MC, Mota-Filipe H, Cuzzocrea S, Pisano B, et al. (2002). Ligands of the peroxisome proliferator-activated receptors (PPAR-gamma and PPAR-alpha) reduce myocardial infarct size. FASEB J 16(9): 1027-1040. Westerhof N, Sipkema P, van den Bos GC, Elzinga G (1972). Forward and backward waves in the arterial system. Cardiovasc Res 6(6): 648-656. Wild S, Roglic G, Green A, Sicree R, King H (2004). Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care 27(5): 1047-1053. Xu Y, Lu L, Greyson C, Rizeq M, Nunley K, Wyatt B, et al. (2006). The PPAR-alpha activator fenofibrate fails to provide myocardial protection in ischemia and reperfusion in pigs. Am J Physiol Heart Circ Physiol 290(5): H1798-1807. Yagi K (1998). Simple assay for the level of total lipid peroxides in serum or plasma. Methods Mol Biol 108: 101-106. Yamashita H, Itsuki A, Kimoto M, Hiemori M, Tsuji H (2006). Acetate generation in rat liver mitochondria; acetyl-CoA hydrolase activity is demonstrated by 3-ketoacyl-CoA thiolase. Biochim Biophys Acta 1761(1): 17-23. Yang TL, Chen MF, Luo BL, Yu J, Jiang JL, Li YJ (2004). Effect of fenofibrate on LDL-induced endothelial dysfunction in rats. Naunyn Schmiedebergs Arch Pharmacol 370(2): 79-83. Yu GS, Lu YC, Gulick T (1998). Co-regulation of tissue-specific alternative human carnitine palmitoyltransferase Ibeta gene promoters by fatty acid enzyme substrate. J Biol Chem 273(49): 32901-32909. Yu K, Bayona W, Kallen CB, Harding HP, Ravera CP, McMahon G, et al. (1995). Differential activation of peroxisome proliferator-activated receptors by eicosanoids. J Biol Chem 270(41): 23975-23983. Yue TL, Bao W, Jucker BM, Gu JL, Romanic AM, Brown PJ, et al. (2003). Activation of peroxisome proliferator-activated receptor-alpha protects the heart from ischemia/reperfusion injury. Circulation 108(19): 2393-2399. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/47097 | - |
| dc.description.abstract | 研究背景與目的：糖尿病人調節醣類及脂肪代謝的功能出現異常，增加心臟對脂肪酸的利用作為能量來源。長期處於如高三酸甘油酯血症這樣的代謝改變會加劇糖尿病人心肌缺血的病徵並降低心肌功能。Peroxisome Proliferator–Activated Receptors (PPARs)被認為可能可用以治療糖尿病、高血脂及動脈硬化等代謝疾病，其中PPARα特別具有改善因代謝異常或糖尿病所引起的高血脂症狀，然而在治療糖尿病心臟功能的作用上，PPARα卻表現出物種特異性的情形。Fenofibrate (Feno)是一種PPARα的致效劑，目前已證實可改善高血脂，另外在血管方面亦具有抑制發炎反應及預防動脈硬化的作用。本篇將利用主動脈輸入阻抗頻譜分析方法，評估Feno在streptozotocin (STZ)誘發之糖尿病大鼠身上，對其動脈管物理特性所造成之影響。
研究方法：隨機將兩個月大之Wistar-Kyoto大鼠分成四組：(i)正常組(NC)；(ii)正常組餵食Feno (NC+Feno)；(iii)STZ誘發之糖尿病組(DM)；(iv)糖尿病餵食Feno組(DM +Feno)。以尾靜脈注射STZ(55mg kg-1)誘發大鼠產生糖尿病，待其出現高血糖症狀，給予餵食組大鼠每日灌食Feno(100mg kg-1)，連續給藥8週並與同齡未給藥之糖尿病控制組做對照，同步記錄大鼠主動脈血壓及血流訊號，以動脈系統的阻抗頻譜分析，接著利用主動脈輸入阻抗頻譜脈衝分析技術取得動脈波反射的相關數據。實驗後採集血液樣本進行血漿中三酸甘油酯、游離脂肪酸、總膽固醇的含量分析，並以硫代巴比妥酸反應物質進行丙二醛的含量分析。 研究結果：與糖尿病控制組相較之下，長期餵食糖尿病鼠Feno在血壓參數、心跳速率、心輸出量及周邊總阻力皆無顯著差異。另外，Feno會增加糖尿病鼠主動脈的特徵阻抗，然而對主動脈容積度並無影響。而在波反射現象方面，Feno會降低因糖尿病所上升的波反射係數達32.4%( p<0.001)，意味著長期餵食糖尿病鼠Feno可延遲脈波反射返回的現象，此結果亦可從波傳輸時間上升了21.1%(p<0.001)得到驗證。而由波傳輸時間的顯著上升及波反射係數的顯著下降的結果顯示，Feno可能可以減輕因糖尿病所導致的左心室收縮負荷的惡化，並藉由減輕糖尿病所引起的收縮負荷來預防心臟肥厚的現象，此可由左心室重量對體重的比值有顯著下降的結果證實。另外亦觀察到給予糖尿病鼠Feno可降低血漿中的三酸甘油酯及游離脂肪酸，以及降低血漿與主動脈中的丙二醛含量。 結論：長期給予Feno治療以STZ誘發之糖尿病大鼠，可減輕其主動脈收縮負荷及改善心臟肥厚的現象，可能與降低血漿中的三酸甘油酯及游離脂肪酸，並降低血漿中及主動脈中的脂質氧化物丙二醛有關。 | zh_TW |
| dc.description.abstract | Background and purpose：Patients with diabetes have disturbances in the regulation of carbohydrate and fat metabolism, leading to an impaired cardiac glucose oxidation and a greater uptake and utilization of free fatty acids. These metabolic changes by prolonged hyperglycemia are responsible for both the increased susceptibility of the diabetic heart to myocardial ischemia and greater decrease of myocardial performance. Peroxisome proliferator–activated receptors (PPARs) are promising targets for the development of new drugs, which treat metabolic disorders such as diabetes, dyslipidemia and atherosclerosis. Although activation of the nuclear receptor, PPAR-α, exerts species-specific activities in the diabetic heart, PPAR-α activators appear to be particularly indicated to treat dyslipidemia of the metabolic syndrome and diabetes mellitus. Fenofibrate (Feno), a PPAR-α agonist, has been demonstrated to improve dyslipidemia, inhibiting proinflammatory and proatherogenic responses in the vasculature. The present study focused on investigating the effects of Feno on the physical properties of the arterial system in streptozotocin (STZ)-induced diabetic in rats, using aortic input impedance analysis.
Methods：Male Wistar rats at two months were randomly divided into four groups as follows：(i) normal control (NC)；(ii) NC treated with Feno (NC+Feno)；(iii) STZ-induced diabetic rats (DM)；(iv) DM treated with Feno (DM+Feno). Diabetes was induced in animals by a single tail vein injection with 55mg kg-1 STZ. After development of hyperglycemia, rats were treated for 8 weeks with Fenofibrate (100 mg kg-1) by oral gavage and compared with the age-matched untreated diabetic controls. Pulsatile aortic pressure and flow signals were measured to perform the vascular impedance analysis. Arterial wave reflection was derived using the impulse response function of the filtered aortic input impedance spectra. At the end of catheterization, blood samples from the animals studied were collected for determination of plasma levels of triglyceride (TG), free fatty acid (FFA), and total cholesterol. Thiobarbituric acid reactive substances (TBARS) measurement was used to estimate malondialdehyde (MDA) content. Results：Feno produced no significant changes in pressure parameters, basal heart rate, cardiac output and total peripheral resistance in the DM. On the other hand, aortic characteristic impedance but not systemic arterial compliance was increased in response to treatment of the STZ-diabetic rats with Feno. As for wave reflection phenomena, Feno attenuated the diabetes-related augmentation in wave reflection factor by 32.4%( p<0.001). Long-term administration of Feno to the STZ-diabetic animals also resulted in a delay return of the pulse wave reflection, as evidenced by the increase of 21.1% in wave transit time( p<0.001). A significant increase in wave transit time and a decrease in wave reflection factor suggested that Feno may alleviate the diabetes-induced deterioration in systolic loading condition for the left ventricle (LV). The decline in systolic load by Feno treatment could be responsible for the prevention of cardiac hypertrophy in the DM, as manifested by the fall of LV weight-body weight ratio. This was in parallel with its lowering of TG and FFA levels in plasma and MDA/TBARS content in plasma and aortic walls in diabetes. Conclusion：Long-term treatment of the STZ-diabetic rats with Feno attenuates aortic systolic load and cardiac hypertrophy, possibly through its decrease of TG and FFA levels in plasma and lipid oxidation-derived MDA/TBARS content in plasma and aortic walls. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T05:47:29Z (GMT). No. of bitstreams: 1 ntu-100-R98441019-1.pdf: 1165218 bytes, checksum: 9572b4234d22071200e99e4b7a4a22b7 (MD5) Previous issue date: 2011 | en |
| dc.description.tableofcontents | 目錄...................................................................................................................................ii
縮寫名詞對照表............................................................................................................ .vi 中文摘要........................................................................................................................viii 英文摘要...........................................................................................................................x 表次................................................................................................................................xiii 圖次................................................................................................................................xiv 文獻回顧 一、糖尿病 1-1糖尿病流行病學.................................................................................................1 1-2糖尿病分類與簡介....................................................................... .....................1 1-3糖尿病對血管的影響................................................................... .....................2 1-4糖尿病對心臟的影響................................................................... .....................4 二、PPARs 2-1 PPARs簡介.........................................................................................................5 2-2 PPARα的功能與表現.........................................................................................5 2-3 PPARα的功能-促進脂肪代謝...........................................................................6 2-4 PPARα的功能-抗發炎反應...............................................................................7 2-5 PPARα與動脈粥狀硬化....................................................................................7 2-6 PPARα與心肌缺血……....................................................................................8 2-7 PPARα致效劑-Fenofibrate................................................................................8 三、動脈物理性質之量化 3-1主動脈輸入阻抗頻譜的特性及功能...............................................................10 研究目的.........................................................................................................................12 材料與方法 一、實驗動物製備.........................................................................................................13 二、實驗動物分組.........................................................................................................13 三、實驗儀器介紹 3-1壓力感應器.......................................................................................................14 3-2電磁感應血流計...............................................................................................14 四、實驗流程..................................................................................................................15 五、左心室比率.............................................................................................................16 六、資料轉換與分析方法 6-1平均週期運算法則...........................................................................................17 6-2時序校正...........................................................................................................18 6-3血行力學參數之計算與分析 6-3-1主動脈輸入阻抗頻譜..............................................................................18 6-3-2動脈容積度..............................................................................................21 6-3-3前進波、反射波與波反射係數推算........................................................21 6-3-4波傳輸時間的推算..................................................................................22 七、生化物質的檢測 7-1三酸甘油酯的檢測...........................................................................................22 7-2游離脂肪酸的檢測...........................................................................................23 7-3膽固醇的檢測...................................................................................................23 7-4丙二醛/硫代巴比妥酸反應物質的檢測..........................................................24 八、統計方法.................................................................................................................25 結果 一、基本資料.................................................................................................................26 二、主動脈輸入阻抗頻譜...............................................................................................26 三、穩態血行力學參數...................................................................................................27 四、脈態血行力學參數...................................................................................................27 五、生化物質.................................................................................................................28 討論 一、糖尿病及餵食Feno對心血管動脈物理特性之影響 1-1基本資料...........................................................................................................30 1-2穩態參數部分...................................................................................................31 1-3脈態參數部分 1-3-1波傳輸時間與波反射係數......................................................................33 1-3-2主動脈特徵阻抗......................................................................................34 1-3-3主動脈容積度..........................................................................................35 二、糖尿病及餵食fenofibrate對血漿生化物質之影響..............................................35 結論........................................................................................ ........................................37 實驗限制.................................................................... ....................................................38 表次 表一：糖尿病及投予Fenofibrate對於雄性Wistar大鼠之血糖、體重、左心室重量以及主動脈血壓相關數據之影響............................ ....................................................39 圖次 圖一：升主動脈特徵阻抗頻譜之振幅、相位及脈衝響應.........................................40圖二：糖尿病及投予Fenofibrate對雄性Wistar大鼠之心跳速率(HR，圖A)、心 輸出量(CO，圖B)、心搏量(SV，圖C)及周邊總阻力(Rp，圖D)的影響.........................41 圖三：糖尿病及投予Feno對雄性Wistar大鼠之主動脈特徵阻抗(Zc，圖A)、主 動脈容積度(Cm，圖B)、波反射係數(Rf，圖C)及波傳輸時間(τ，圖D)的影響.....42 圖四：糖尿病及投予Feno對雄性Wistar大鼠之血漿中之三酸甘油酯(TG，圖A)、 游離脂肪酸(FFA，圖B)及總膽固醇(total cholesterol，圖C)的影響.........................43 圖五：糖尿病及投予Feno對雄性Wistar大鼠之血漿中丙二醛/硫代巴比妥酸反應物 質(malondialdehyde / thiobarbituric acid reactive substances, MDA / TBARS，圖A)及主動脈中丙二醛/硫代巴比妥酸反應物質的含量(圖B) 的影響................................44 參考文獻.................................................................... ....................................................45 | |
| dc.language.iso | zh-TW | |
| dc.subject | 丙二醛 | zh_TW |
| dc.subject | PPARα | zh_TW |
| dc.subject | Fenofibrate | zh_TW |
| dc.subject | STZ誘發之糖尿病鼠 | zh_TW |
| dc.subject | 主動脈輸入阻抗頻譜分析 | zh_TW |
| dc.subject | 總膽固醇 | zh_TW |
| dc.subject | 游離脂肪酸 | zh_TW |
| dc.subject | 三酸甘油酯 | zh_TW |
| dc.subject | Fenofibrate | en |
| dc.subject | STZ-induced diabetic rats | en |
| dc.subject | PPARα | en |
| dc.subject | MDA | en |
| dc.subject | triglyceride | en |
| dc.subject | free fatty acid | en |
| dc.subject | t-cholesterol | en |
| dc.subject | aortic input impedance analysis | en |
| dc.title | Fenofibrate對streptozotocin所誘發糖尿病鼠之動脈系統物理性質的影響 | zh_TW |
| dc.title | Effects of fenofibrate on mechanical properties of arterial system in streptozotocin-induced diabetic rats | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 99-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 吳明修(Ming-Shiou Wu),陳文彬 | |
| dc.subject.keyword | PPARα,Fenofibrate,STZ誘發之糖尿病鼠,主動脈輸入阻抗頻譜分析,總膽固醇,游離脂肪酸,三酸甘油酯,丙二醛, | zh_TW |
| dc.subject.keyword | PPARα,Fenofibrate,STZ-induced diabetic rats,aortic input impedance analysis,t-cholesterol,free fatty acid,triglyceride,MDA, | en |
| dc.relation.page | 58 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2011-08-19 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 生理學研究所 | zh_TW |
| 顯示於系所單位： | 生理學科所 | |
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