Fibraty – rola i mechanizmy działania hipolipemizującego Artykuł przeglądowy
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Opublikowane:
gru 31, 2015
Słowa kluczowe:
hipertriglicerydemia, fibraty, PPAR, dyslipidemia
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Abstrakt
Zaburzenia lipidowe są szeroko rozpowszechnionym czynnikiem ryzyka sercowo-naczyniowego w Polsce. Do grupy podstawowych leków stosowanych w leczeniu dyslipidemii, oprócz statyn, zalicza się fibraty. Ich stosowanie jako leku podstawowego lub dodatkowego jest wskazane w dyslipidemiach z podwyższonym stężeniem triglicerydów. Do tej pory mechanizm działania fibratów nie został do końca poznany, jednak najnowsze badania wskazują na udział receptorów jądrowych z rodziny PPAR. W artykule przedstawiono wskazania do stosowania fibratów, podstawowe zasady leczenia nimi oraz mechanizm działania tych leków w odniesieniu do fizjologicznej roli receptorów PPAR.
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Jak cytować
Sobieraj , P., Lewandowski , J., Dęmbe , K., & Krasnodębski , P. (2015). Fibraty – rola i mechanizmy działania hipolipemizującego . Medycyna Faktów , 8(4(29), 24-30. Pobrano z https://journalsmededu.pl/index.php/jebm/article/view/2279
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Bibliografia
1. Wożakowska-Kapłon B., Filipiak K., Mamcarz A. et al.: Aktualne problemy terapii dyslipidemii w Polsce – II Deklaracja Sopocka. Kardiol. Pol. 2014; 72(9): 847-885.
2. Reiner Z., Catapano A.L., Backer G.D. et al.: ESC/EAS Guidelines for the management of dyslipidaemias. Eur. Heart J. 2011; 32: 1769-1818.
3. Hypertriglyceridaemia and vascular risk. Report of a meeting of physicians and scientists, University College London Medical School. Lancet 1993; 342: 781-787.
4. Brunzell J.D.: Clinical practice. Hypertriglyceridemia. N. Engl. J. Med. 2007; 357: 1009-1017.
5. DeFronzo R.A., Ferrannini E.: Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991; 14: 173-194.
6. Simpson H.C., Mann J.I., Meade T.W. et al.: Hypertriglyceridaemia and hypercoagulability. Lancet 1983; 1: 786-790.
7. Sarwar N., Danesh J., Eiriksdottir G. et al.: Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation 2007; 115: 450-458.
8. Sprecher D.L., Pearce G.L., Cosgrove D.M. et al.: Relation of serum triglyceride levels to survival after coronary artery bypass grafting. Am. J. Cardiol. 2000; 86: 285-288.
9. Staels B., Dallongeville J., Auwerx J. et al.: Mechanism of action of fibrates on lipid and lipoprotein metabolism. Circulation 1998; 98: 2088-2093.
10. Jin F.Y., Kamanna V.S., Chuang M.Y. et al.: Gemfibrozil stimulates apolipoprotein A-I synthesis and secretion by stabilization of mRNA transcripts in human hepatoblastoma cell line (Hep G2). Arterioscler. Thromb. Vasc. Biol. 1996; 16: 1052-1062.
11. Vu-Dac N., Schoonjans K., Kosykh V. et al.: Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator- activated receptor. J. Clin. Invest. 1995; 96: 741-750.
12. Rosenson R.S., Wolff D.A., Huskin A.L. et al.: Fenofibrate therapy ameliorates fasting and postprandial lipoproteinemia, oxidative stress, and the inflammatory response in subjects with hypertriglyceridemia and the metabolic syndrome. Diabetes Care 2007; 30: 1945-1951.
13. Frick M.H., Elo O., Haapa K. et al.: Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. N. Engl. J. Med. 1987; 317: 1237-1245.
14. Rubins H.B., Robins S.J., Collins D. et al.: 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. 1999; 341: 410-418.
15. Keech A., Simes R.J., Barter P. et al.; The FIELD Study Investigators: Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005; 366: 1849-1861.
16. The ACCORD Study Group: Effects of combination lipid therapy in type 2 diabetes mellitus. N. Engl. J. Med. 2010; 362: 1563-1574.
17. Wanders R.J.: Metabolic functions of peroxisomes in health and disease. Biochimie 2014; 98: 36-44.
18. Varga T., Czimmerer Z., Nagy L.: PPARs are a unique set of fatty acid regulated transcription factors controlling both lipid metabolism and inflammation. Biochimica et Biophysica Acta 2011; 1812: 1007-1022.
19. Hamblin M., Chang L., Fan Y. et al.: PPARs and the cardiovascular system. Antioxid. Redox Signal. 2009; 11(6): 1415-1452.
20. Stolarczyk M., Gutman W., Derlacz R.A.: Receptory jądrowe PPAR jako miejsce działania leków w zaburzeniach metabolicznych. Postępy Biochemii 2011; 57(2): 207-214.
21. A co-operative trial in the primary prevention of ischaemic heart disease using clofibrat. Report from the Commitee of Principal Investigators: Br. Heart J. 1987; 40: 1069-1118.
22. Shephard J.: The fibrates in clinical practice: focus on micronized fenofibrate. Atherosclerosis 1994; 110: S55-63.
2. Reiner Z., Catapano A.L., Backer G.D. et al.: ESC/EAS Guidelines for the management of dyslipidaemias. Eur. Heart J. 2011; 32: 1769-1818.
3. Hypertriglyceridaemia and vascular risk. Report of a meeting of physicians and scientists, University College London Medical School. Lancet 1993; 342: 781-787.
4. Brunzell J.D.: Clinical practice. Hypertriglyceridemia. N. Engl. J. Med. 2007; 357: 1009-1017.
5. DeFronzo R.A., Ferrannini E.: Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991; 14: 173-194.
6. Simpson H.C., Mann J.I., Meade T.W. et al.: Hypertriglyceridaemia and hypercoagulability. Lancet 1983; 1: 786-790.
7. Sarwar N., Danesh J., Eiriksdottir G. et al.: Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation 2007; 115: 450-458.
8. Sprecher D.L., Pearce G.L., Cosgrove D.M. et al.: Relation of serum triglyceride levels to survival after coronary artery bypass grafting. Am. J. Cardiol. 2000; 86: 285-288.
9. Staels B., Dallongeville J., Auwerx J. et al.: Mechanism of action of fibrates on lipid and lipoprotein metabolism. Circulation 1998; 98: 2088-2093.
10. Jin F.Y., Kamanna V.S., Chuang M.Y. et al.: Gemfibrozil stimulates apolipoprotein A-I synthesis and secretion by stabilization of mRNA transcripts in human hepatoblastoma cell line (Hep G2). Arterioscler. Thromb. Vasc. Biol. 1996; 16: 1052-1062.
11. Vu-Dac N., Schoonjans K., Kosykh V. et al.: Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator- activated receptor. J. Clin. Invest. 1995; 96: 741-750.
12. Rosenson R.S., Wolff D.A., Huskin A.L. et al.: Fenofibrate therapy ameliorates fasting and postprandial lipoproteinemia, oxidative stress, and the inflammatory response in subjects with hypertriglyceridemia and the metabolic syndrome. Diabetes Care 2007; 30: 1945-1951.
13. Frick M.H., Elo O., Haapa K. et al.: Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. N. Engl. J. Med. 1987; 317: 1237-1245.
14. Rubins H.B., Robins S.J., Collins D. et al.: 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. 1999; 341: 410-418.
15. Keech A., Simes R.J., Barter P. et al.; The FIELD Study Investigators: Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005; 366: 1849-1861.
16. The ACCORD Study Group: Effects of combination lipid therapy in type 2 diabetes mellitus. N. Engl. J. Med. 2010; 362: 1563-1574.
17. Wanders R.J.: Metabolic functions of peroxisomes in health and disease. Biochimie 2014; 98: 36-44.
18. Varga T., Czimmerer Z., Nagy L.: PPARs are a unique set of fatty acid regulated transcription factors controlling both lipid metabolism and inflammation. Biochimica et Biophysica Acta 2011; 1812: 1007-1022.
19. Hamblin M., Chang L., Fan Y. et al.: PPARs and the cardiovascular system. Antioxid. Redox Signal. 2009; 11(6): 1415-1452.
20. Stolarczyk M., Gutman W., Derlacz R.A.: Receptory jądrowe PPAR jako miejsce działania leków w zaburzeniach metabolicznych. Postępy Biochemii 2011; 57(2): 207-214.
21. A co-operative trial in the primary prevention of ischaemic heart disease using clofibrat. Report from the Commitee of Principal Investigators: Br. Heart J. 1987; 40: 1069-1118.
22. Shephard J.: The fibrates in clinical practice: focus on micronized fenofibrate. Atherosclerosis 1994; 110: S55-63.