Aerobic Exercise Training Reduces Atherogenesis Induced by Low-Sodium Diet in LDL Receptor Knockout Mice
Carregando...
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2022
Título da Revista
ISSN da Revista
Título do Volume
Editora
MDPI
Autores
PINTO, Paula Ramos
RODRIGUES, Leticia Gomes
TREVISANI, Mayara da Silva
SILVA, Alexandre Alves da
Citação
ANTIOXIDANTS, v.11, n.10, article ID 2023, 16p, 2022
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
- Adams V, 2005, CIRCULATION, V111, P555, DOI 10.1161/01.CIR.0000154560.88933.7E
- Alderman MH, 2010, JAMA-J AM MED ASSOC, V303, P448, DOI 10.1001/jama.2010.69
- Bond AR, 2011, J BIOMED BIOTECHNOL, DOI 10.1155/2011/379069
- Catanozi S, 2003, J LIPID RES, V44, P727, DOI 10.1194/jlr.M200330-JLR200
- Catanozi S, 2001, ATHEROSCLEROSIS, V158, P81, DOI 10.1016/S0021-9150(01)00415-4
- Centa M, 2019, JOVE-J VIS EXP, DOI 10.3791/59828
- Cook NR, 2016, J AM COLL CARDIOL, V68, P1609, DOI 10.1016/j.jacc.2016.07.745
- da Silva KS, 2017, FRONT PHYSIOL, V8, DOI 10.3389/fphys.2017.00723
- Dikalov SI, 2014, ANTIOXID REDOX SIGN, V20, P281, DOI 10.1089/ars.2012.4918
- Drinane M, 2009, CIRC RES, V104, P337, DOI 10.1161/CIRCRESAHA.108.184622
- Eto H, 2008, HYPERTENS RES, V31, P1631, DOI 10.1291/hypres.31.1631
- Ferreira GD, 2021, NUTRIENTS, V13, DOI 10.3390/nu13072174
- Ferreira JCB, 2007, CLIN EXP PHARMACOL P, V34, P760, DOI 10.1111/j.1440-1681.2007.04635.x
- Flynn MG, 2006, EXERC SPORT SCI REV, V34, P176, DOI 10.1249/01.jes.0000240027.22749.14
- Fusco FB, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0177086
- Gabriel BM, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0082669
- Garg R, 2011, METABOLISM, V60, P965, DOI 10.1016/j.metabol.2010.09.005
- Gomes DJ, 2016, J DIABETES COMPLICAT, V30, P1614, DOI 10.1016/j.jdiacomp.2016.07.001
- Gu Q, 2014, CARDIOVASC PATHOL, V23, P298, DOI 10.1016/j.carpath.2014.05.006
- Hardie DG, 2012, NAT REV MOL CELL BIO, V13, P251, DOI 10.1038/nrm3311
- ISHIBASHI S, 1993, J CLIN INVEST, V92, P883, DOI 10.1172/JCI116663
- Ivanovski O, 2005, ATHEROSCLEROSIS, V180, P271, DOI 10.1016/j.atherosclerosis.2004.12.020
- Jayedi A, 2019, CLIN NUTR, V38, P1092, DOI 10.1016/j.clnu.2018.05.017
- Kadoglou NPE, 2013, EUR J HISTOCHEM, V57, P16, DOI 10.4081/ejh.2013.e3
- Kahn BB, 2005, CELL METAB, V1, P15, DOI 10.1016/j.cmet.2004.12.003
- Kamioka M, 2010, J ATHEROSCLER THROMB, V17, P590, DOI 10.5551/jat.3624
- Kawanishi N, 2010, EXERC IMMUNOL REV, V16, P105
- LASSEGUE B, 1995, MOL PHARMACOL, V48, P601
- Lee SH, 2019, CHEM RES TOXICOL, V32, P1412, DOI 10.1021/acs.chemrestox.9b00110
- Linder AE, 2007, J PHARMACOL EXP THER, V323, P78, DOI 10.1124/jpet.107.123463
- Maier T, 2009, FEBS LETT, V583, P3966, DOI 10.1016/j.febslet.2009.10.036
- Muscogiuri G, 2008, CURR VASC PHARMACOL, V6, P301, DOI 10.2174/157016108785909715
- Nickenig G, 2000, BRIT J PHARMACOL, V131, P795, DOI 10.1038/sj.bjp.0703623
- Ogihara T, 2002, HYPERTENSION, V40, P872, DOI 10.1161/01.HYP.0000040262.48405.A8
- Ohgami Nobutaka, 2003, J Atheroscler Thromb, V10, P1
- Olivares-Reyes JA, 2009, MOL CELL ENDOCRINOL, V302, P128, DOI 10.1016/j.mce.2008.12.011
- Oliveira M, 2010, EUR J APPL PHYSIOL, V109, P251, DOI 10.1007/s00421-009-1350-9
- Pedersen BK, 2012, NAT REV ENDOCRINOL, V8, P457, DOI 10.1038/nrendo.2012.49
- Pedersen BK, 2006, ESSAYS BIOCHEM, V42, P105, DOI 10.1042/bse0420105
- Pellegrin M, 2009, HYPERTENSION, V53, P782, DOI 10.1161/HYPERTENSIONAHA.108.128165
- Petersen AMW, 2005, J APPL PHYSIOL, V98, P1154, DOI 10.1152/japplphysiol.00164.2004
- Pickering RJ, 2019, J CLIN INVEST, V129, P406, DOI 10.1172/JCI99987
- Pinto PR, 2021, J BIOL CHEM, V296, DOI 10.1016/j.jbc.2021.100344
- Pinto DC, 2018, SCI REP-UK, V8, DOI 10.1038/s41598-018-26482-6
- Rocco DDFM, 2011, LIPIDS, V46, P617, DOI 10.1007/s11745-011-3555-z
- Rockl KSC, 2008, IUBMB LIFE, V60, P145, DOI 10.1002/iub.21
- Roque FR, 2013, CURR HYPERTENS REP, V15, P204, DOI 10.1007/s11906-013-0336-5
- Rosenfeld ME, 2008, CURR DRUG TARGETS, V9, P210, DOI 10.2174/138945008783755575
- Simo OK, 2017, CAN J PHYSIOL PHARM, V95, P977, DOI 10.1139/cjpp-2017-0170
- SINZINGER H, 1988, SPORTS MED, V6, P238, DOI 10.2165/00007256-198806040-00005
- Stanford KI, 2014, ADV PHYSIOL EDUC, V38, P308, DOI 10.1152/advan.00080.2014
- Stefano GB, 2001, INT J MOL MED, V7, P119
- Tabas I, 2015, J CELL BIOL, V209, P13, DOI 10.1083/jcb.201412052
- Thomas MC, 2005, J AM SOC NEPHROL, V16, P2976, DOI 10.1681/ASN.2005010013
- Thomas WG, 1999, REGUL PEPTIDES, V79, P9, DOI 10.1016/S0167-0115(98)00140-2
- Tikellis C, 2012, HYPERTENSION, V60, P98, DOI 10.1161/HYPERTENSIONAHA.112.191767
- Timmerman KL, 2008, J LEUKOCYTE BIOL, V84, P1271, DOI 10.1189/jlb.0408244
- Veseli BE, 2017, EUR J PHARMACOL, V816, P3, DOI 10.1016/j.ejphar.2017.05.010
- Vogel C, 2012, NAT REV GENET, V13, P227, DOI 10.1038/nrg3185
- Wassmann S, 2006, J HYPERTENS, V24, pS15, DOI 10.1097/01.hjh.0000220402.53869.72
- Williams H, 2002, ARTERIOSCL THROM VAS, V22, P788, DOI 10.1161/01.ATV.0000014587.66321.B4
- Xu L, 2019, CIRC J, V83, P1954, DOI 10.1253/circj.CJ-19-0153
- Yokoyama S, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-85312-4
- Yu MG, 2017, INT J MOL SCI, V18, DOI 10.3390/ijms18061260
- Zheng FP, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0101269