Lipid transfers to HDL are diminished in long-term bedridden patients: association with low HDL-cholesterol and increased inflammatory markers

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art_OLIVEIRA_Lipid_transfers_to_HDL_are_diminished_in_longterm_2017.PDF (432.63 KB)
Citações na Scopus
2
Tipo de produção
article
Data de publicação
2017
Editora
SPRINGER HEIDELBERG
DOI
Indexadores
Scopus
Web of Science
PubMed
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Título do Volume
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Autor de Grupo de pesquisa
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Citação
LIPIDS, v.52, n.8, p.703-709, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Plasma lipids have been extensively studied in sedentary and in subjects practicing exercise training, but not in extreme inactivity as occurs in bedridden patients. This is important for the care of bedridden patients and understanding the overall plasma lipid regulation. Here, we investigated plasma lipids, lipid transfers to HDL and inflammatory markers in bedridden patients. Fasting blood samples were collected from 23 clinically stable bedridden patients under long-term care (> 90 days) and 26 normolipidemic sedentary subjects, paired for age and gender. In vitro transfer of four lipids to HDL was performed by incubating plasma with donor nanoparticles containing radioactive lipids. Total (193 +/- 36 vs 160 +/- 43, p = 0.005), LDL (124 +/- 3 vs 96 +/- 33 p = 0.003) and HDL-cholesterol (45 +/- 10 vs 36 +/- 13, p = 0.008), apolipoprotein A-I (134 +/- 20 vs 111 +/- 24, p = 0.001) and oxidized LDL (53 +/- 13 vs 43 +/- 12, p = 0.011) were lower in bedridden patients, whereas triglycerides, apolipoprotein B, CETP and LCAT were equal in both groups. Transfers of all lipids, namely unesterified cholesterol, cholesterol esters, triglycerides and phospholipids, to HDL were lower in bedridden patients, probably due to their lower HDL-cholesterol levels. Concentrations of IL-1 beta, IL-6, IL-8, HGF and NGF were higher in bedridden patients compared to sedentary subjects. In conclusion, inactivity had great impact on HDL, by lowering HDL-cholesterol, apolipoprotein A-I and thereby cholesterol transfers to the lipoprotein, which suggests that inactivity may deteriorate HDL protection beyond the ordinary sedentary condition.
Palavras-chave
High-density lipoproteins (HDL), Lipid metabolism, Cholesterol ester transfer protein (CETP), Exercise training, Nanoparticles
URI
https://observatorio.fm.usp.br/handle/OPI/22123
Referências
  1. Albers JJ, 2012, BBA-MOL CELL BIOL L, V1821, P345, DOI 10.1016/j.bbalip.2011.06.013
  2. Bachi ALL, 2015, J AM GERIATR SOC, V63, P1247, DOI 10.1111/jgs.13500
  3. Bank M, 2015, ARCH PHYS MED REHAB, V96, P633, DOI 10.1016/j.apmr.2014.10.021
  4. Barter P, 2000, ARTERIOSCL THROM VAS, V20, P2029
  5. Barter P, 2003, ATHEROSCLEROSIS, V168, P195, DOI 10.1016/S0021-9150(03)00006-6
  6. Burger Danielle, 2002, Autoimmunity Reviews, V1, P111, DOI 10.1016/S1568-9972(01)00018-0
  7. Casella A, 2011, AM J CARDIOL, V107, P1168, DOI 10.1016/j.amjcard.2010.12.014
  8. da Silva JL, 2011, ATHEROSCLEROSIS, V219, P532, DOI 10.1016/j.atherosclerosis.2011.08.014
  9. Davies AL, 2007, ARCH PHYS MED REHAB, V88, P1384, DOI 10.1016/j.apmr.2007.08.004
  10. Dullaart RPF, 2013, OBESITY, V21, P361, DOI 10.1002/oby.20058
  11. Durstine J Larry, 2002, J Cardiopulm Rehabil, V22, P385, DOI 10.1097/00008483-200211000-00002
  12. Falk E, 2006, J AM COLL CARDIOL, V47, pC7, DOI 10.1016/j.jacc.2005.09.068
  13. GINSBURG GS, 1982, J BIOL CHEM, V257, P8216
  14. Halverstadt A, 2007, METABOLISM, V56, P444, DOI 10.1016/j.metabol.2006.10.019
  15. Huuskonen J, 2001, ATHEROSCLEROSIS, V155, P269, DOI 10.1016/S0021-9150(01)00447-6
  16. Jung RT, 1997, BRIT MED BULL, V53, P307
  17. Kwon BK, 2010, J NEUROTRAUM, V27, P669, DOI 10.1089/neu.2009.1080
  18. Lee IM, 2012, LANCET, V380, P219, DOI 10.1016/S0140-6736(12)61031-9
  19. Levitan I, 2010, ANTIOXID REDOX SIGN, V13, P39, DOI 10.1089/ars.2009.2733
  20. Lira FS, 2010, DIABETOL METAB SYNDR, V22, P2
  21. Lo Prete AC, 2009, LIPIDS, V44, P917, DOI 10.1007/s11745-009-3342-2
  22. MACKAY AG, 1990, BIOCHEM J, V269, P123
  23. Maranhao RC, 2014, ADV CLIN CHEM, V65, P1, DOI 10.1016/B978-0-12-800141-7.00001-2
  24. Maranhao RC, 2012, CLIN CHIM ACTA, V413, P502, DOI 10.1016/j.cca.2011.11.011
  25. MARANHAO RC, 1993, LIPIDS, V28, P691, DOI 10.1007/BF02535988
  26. Marsche G, 2013, PHARMACOL THERAPEUT, V137, P341, DOI 10.1016/j.pharmthera.2012.12.001
  27. Navab M, 2006, NAT CLIN PRACT ENDOC, V2, P504, DOI 10.1038/ncpendmet0245
  28. Parthasarathy S, 2010, METHODS MOL BIOL, V610, P403, DOI 10.1007/978-1-60327-029-8_24
  29. PORAT O, 1989, LYMPHOKINE RES, V8, P459
  30. Rousset X, 2011, CURR ATHEROSCLER REP, V13, P249, DOI 10.1007/s11883-011-0171-6
  31. Sprandel MCO, 2015, CARDIOVASC DIABETOL, V14, DOI 10.1186/s12933-015-0270-8
  32. Tolle M, 2012, CARDIOVASC RES, V94, P154, DOI 10.1093/cvr/cvs089
  33. Vaisberg M, 2012, LIPIDS, V47, P679, DOI 10.1007/s11745-012-3685-y
  34. Vinagre CGC, 2007, J APPL PHYSIOL, V103, P1166, DOI 10.1152/japplphysiol.01176.2006
  35. Wang MH, 2004, CHEM REV, V104, P119, DOI 10.1021/cr020466v
  36. Yang LQ, 2004, SPINE, V29, P966, DOI 10.1097/00007632-200405010-00004
  37. Yu R, 2008, CURR ATHEROSCLER REP, V10, P171, DOI 10.1007/s11883-008-0025-z

Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/31
Artigos e Materiais de Revistas Científicas - ODS/03