Aerobic Exercise Training Reduces Atherogenesis Induced by Low-Sodium Diet in LDL Receptor Knockout Mice

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Citações na Scopus
1
Tipo de produção
article
Data de publicação
2022
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ISSN da Revista
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MDPI
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ANTIOXIDANTS, v.11, n.10, article ID 2023, 16p, 2022
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Unidades Organizacionais
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Resumo
This study investigated the efficacy of aerobic exercise training (AET) in the prevention of dyslipidemia, insulin resistance (IR), and atherogenesis induced by severe low-sodium (LS) diet. LDL receptor knockout (LDLR KO) mice were fed a low-sodium (LS) (0.15% NaCl) or normal-sodium (NS; 1.27% NaCl) diet, submitted to AET in a treadmill, 5 times/week, 60 min/day, 15 m/min, for 90 days, or kept sedentary. Blood pressure (BP), plasma total cholesterol (TC) and triglyceride (TG) concentrations, lipoprotein profile, and insulin sensitivity were evaluated at the end of the AET protocol. Lipid infiltration, angiotensin II type 1 receptor (AT1), receptor for advanced glycation end products (RAGE), carboxymethyllysine (CML), and 4-hydroxynonenal (4-HNE) contents as well as gene expression were determined in the brachiocephalic trunk. BP and TC and gene expression were similar among groups. Compared to the NS diet, the LS diet increased vascular lipid infiltration, CML, RAGE, 4-HNE, plasma TG, LDL-cholesterol, and VLDL-TG. Conversely, the LS diet reduced vascular AT1 receptor, insulin sensitivity, HDL-cholesterol, and HDL-TG. AET prevented arterial lipid infiltration; increases in CML, RAGE, and 4-HNE contents; and reduced AT1 levels and improved LS-induced peripheral IR. The current study showed that AET counteracted the deleterious effects of chronic LS diet in an atherogenesis-prone model by ameliorating peripheral IR, lipid infiltration, CML, RAGE, 4-HNE, and AT1 receptor in the intima-media of the brachiocephalic trunk. These events occurred independently of the amelioration of plasma-lipid profile, which was negatively affected by the severe dietary-sodium restriction.
Palavras-chave
low-sodium diet, atherogenesis, dyslipidemia, aerobic-exercise training, insulin resistance
Referências
  1. Adams V, 2005, CIRCULATION, V111, P555, DOI 10.1161/01.CIR.0000154560.88933.7E
  2. Alderman MH, 2010, JAMA-J AM MED ASSOC, V303, P448, DOI 10.1001/jama.2010.69
  3. Bond AR, 2011, J BIOMED BIOTECHNOL, DOI 10.1155/2011/379069
  4. Catanozi S, 2003, J LIPID RES, V44, P727, DOI 10.1194/jlr.M200330-JLR200
  5. Catanozi S, 2001, ATHEROSCLEROSIS, V158, P81, DOI 10.1016/S0021-9150(01)00415-4
  6. Centa M, 2019, JOVE-J VIS EXP, DOI 10.3791/59828
  7. Cook NR, 2016, J AM COLL CARDIOL, V68, P1609, DOI 10.1016/j.jacc.2016.07.745
  8. da Silva KS, 2017, FRONT PHYSIOL, V8, DOI 10.3389/fphys.2017.00723
  9. Dikalov SI, 2014, ANTIOXID REDOX SIGN, V20, P281, DOI 10.1089/ars.2012.4918
  10. Drinane M, 2009, CIRC RES, V104, P337, DOI 10.1161/CIRCRESAHA.108.184622
  11. Eto H, 2008, HYPERTENS RES, V31, P1631, DOI 10.1291/hypres.31.1631
  12. Ferreira GD, 2021, NUTRIENTS, V13, DOI 10.3390/nu13072174
  13. Ferreira JCB, 2007, CLIN EXP PHARMACOL P, V34, P760, DOI 10.1111/j.1440-1681.2007.04635.x
  14. Flynn MG, 2006, EXERC SPORT SCI REV, V34, P176, DOI 10.1249/01.jes.0000240027.22749.14
  15. Fusco FB, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0177086
  16. Gabriel BM, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0082669
  17. Garg R, 2011, METABOLISM, V60, P965, DOI 10.1016/j.metabol.2010.09.005
  18. Gomes DJ, 2016, J DIABETES COMPLICAT, V30, P1614, DOI 10.1016/j.jdiacomp.2016.07.001
  19. Gu Q, 2014, CARDIOVASC PATHOL, V23, P298, DOI 10.1016/j.carpath.2014.05.006
  20. Hardie DG, 2012, NAT REV MOL CELL BIO, V13, P251, DOI 10.1038/nrm3311
  21. ISHIBASHI S, 1993, J CLIN INVEST, V92, P883, DOI 10.1172/JCI116663
  22. Ivanovski O, 2005, ATHEROSCLEROSIS, V180, P271, DOI 10.1016/j.atherosclerosis.2004.12.020
  23. Jayedi A, 2019, CLIN NUTR, V38, P1092, DOI 10.1016/j.clnu.2018.05.017
  24. Kadoglou NPE, 2013, EUR J HISTOCHEM, V57, P16, DOI 10.4081/ejh.2013.e3
  25. Kahn BB, 2005, CELL METAB, V1, P15, DOI 10.1016/j.cmet.2004.12.003
  26. Kamioka M, 2010, J ATHEROSCLER THROMB, V17, P590, DOI 10.5551/jat.3624
  27. Kawanishi N, 2010, EXERC IMMUNOL REV, V16, P105
  28. LASSEGUE B, 1995, MOL PHARMACOL, V48, P601
  29. Lee SH, 2019, CHEM RES TOXICOL, V32, P1412, DOI 10.1021/acs.chemrestox.9b00110
  30. Linder AE, 2007, J PHARMACOL EXP THER, V323, P78, DOI 10.1124/jpet.107.123463
  31. Maier T, 2009, FEBS LETT, V583, P3966, DOI 10.1016/j.febslet.2009.10.036
  32. Muscogiuri G, 2008, CURR VASC PHARMACOL, V6, P301, DOI 10.2174/157016108785909715
  33. Nickenig G, 2000, BRIT J PHARMACOL, V131, P795, DOI 10.1038/sj.bjp.0703623
  34. Ogihara T, 2002, HYPERTENSION, V40, P872, DOI 10.1161/01.HYP.0000040262.48405.A8
  35. Ohgami Nobutaka, 2003, J Atheroscler Thromb, V10, P1
  36. Olivares-Reyes JA, 2009, MOL CELL ENDOCRINOL, V302, P128, DOI 10.1016/j.mce.2008.12.011
  37. Oliveira M, 2010, EUR J APPL PHYSIOL, V109, P251, DOI 10.1007/s00421-009-1350-9
  38. Pedersen BK, 2012, NAT REV ENDOCRINOL, V8, P457, DOI 10.1038/nrendo.2012.49
  39. Pedersen BK, 2006, ESSAYS BIOCHEM, V42, P105, DOI 10.1042/bse0420105
  40. Pellegrin M, 2009, HYPERTENSION, V53, P782, DOI 10.1161/HYPERTENSIONAHA.108.128165
  41. Petersen AMW, 2005, J APPL PHYSIOL, V98, P1154, DOI 10.1152/japplphysiol.00164.2004
  42. Pickering RJ, 2019, J CLIN INVEST, V129, P406, DOI 10.1172/JCI99987
  43. Pinto PR, 2021, J BIOL CHEM, V296, DOI 10.1016/j.jbc.2021.100344
  44. Pinto DC, 2018, SCI REP-UK, V8, DOI 10.1038/s41598-018-26482-6
  45. Rocco DDFM, 2011, LIPIDS, V46, P617, DOI 10.1007/s11745-011-3555-z
  46. Rockl KSC, 2008, IUBMB LIFE, V60, P145, DOI 10.1002/iub.21
  47. Roque FR, 2013, CURR HYPERTENS REP, V15, P204, DOI 10.1007/s11906-013-0336-5
  48. Rosenfeld ME, 2008, CURR DRUG TARGETS, V9, P210, DOI 10.2174/138945008783755575
  49. Simo OK, 2017, CAN J PHYSIOL PHARM, V95, P977, DOI 10.1139/cjpp-2017-0170
  50. SINZINGER H, 1988, SPORTS MED, V6, P238, DOI 10.2165/00007256-198806040-00005
  51. Stanford KI, 2014, ADV PHYSIOL EDUC, V38, P308, DOI 10.1152/advan.00080.2014
  52. Stefano GB, 2001, INT J MOL MED, V7, P119
  53. Tabas I, 2015, J CELL BIOL, V209, P13, DOI 10.1083/jcb.201412052
  54. Thomas MC, 2005, J AM SOC NEPHROL, V16, P2976, DOI 10.1681/ASN.2005010013
  55. Thomas WG, 1999, REGUL PEPTIDES, V79, P9, DOI 10.1016/S0167-0115(98)00140-2
  56. Tikellis C, 2012, HYPERTENSION, V60, P98, DOI 10.1161/HYPERTENSIONAHA.112.191767
  57. Timmerman KL, 2008, J LEUKOCYTE BIOL, V84, P1271, DOI 10.1189/jlb.0408244
  58. Veseli BE, 2017, EUR J PHARMACOL, V816, P3, DOI 10.1016/j.ejphar.2017.05.010
  59. Vogel C, 2012, NAT REV GENET, V13, P227, DOI 10.1038/nrg3185
  60. Wassmann S, 2006, J HYPERTENS, V24, pS15, DOI 10.1097/01.hjh.0000220402.53869.72
  61. Williams H, 2002, ARTERIOSCL THROM VAS, V22, P788, DOI 10.1161/01.ATV.0000014587.66321.B4
  62. Xu L, 2019, CIRC J, V83, P1954, DOI 10.1253/circj.CJ-19-0153
  63. Yokoyama S, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-85312-4
  64. Yu MG, 2017, INT J MOL SCI, V18, DOI 10.3390/ijms18061260
  65. Zheng FP, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0101269