Association between Diastolic Dysfunction with Inflammation and Oxidative Stress in Females ob/ob Mice

Carregando...
Imagem de Miniatura
Citações na Scopus
12
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
FRONTIERS MEDIA SA
Autores
CONTI, Filipe F.
DIAS, Danielle da Silva
MACHI, Jacqueline F.
PALOMINO, Zaira
CASARINI, Dulce E.
RODRIGUES, Bruno
ANGELIS, Kytia de
Citação
FRONTIERS IN PHYSIOLOGY, v.8, article ID 572, 10p, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Objective: To evaluate autonomic and cardiovascular function, as well as inflammatory and oxidative stress markers in ob/ob female mice. Methods: Metabolic parameters, cardiac function, arterial pressure (AP), autonomic, hormonal, inflammatory, and oxidative stressmarkers were evaluated in 12-weeks female wild-type (WT group) and ob/ob mice (OB group). Results: OB animals showed increased body weight, blood glucose, and triglyceride levels, along with glucose intolerance, when compared to WT animals. Ejection fraction (EF) and AP were similar between groups; however, the OB group presented diastolic dysfunction, as well as an impairment on myocardial performance index. Moreover, the OB group exhibited important autonomic dysfunction and baroreflex sensitivity impairment, when compared to WT group. OB group showed increased Angiotensin II levels in heart and renal tissues; decreased adiponectin and increased inflammatory markers in adipose tissue and spleen. Additionally, OB mice presented a higher damage to proteins and lipoperoxidation and lower activity of antioxidant enzymes in kidney and heart. Correlations were found between autonomic dysfunction with angiotensin II and inflammatory mediators, as well as between inflammation and oxidative stress. Conclusions: Our results showed that female adult ob/ob mice presented discrete diastolic dysfunction accompanied by autonomic disorder, which is associated with inflammation and oxidative stress in these animals.
Palavras-chave
obesity, cardiac dysfunction, autonomic, inflammation, female
Referências
  1. Abraham W. T., 2003, REV CARDIOVASC ME S2, V4, pS30
  2. AMES BN, 1993, P NATL ACAD SCI USA, V90, P7915, DOI 10.1073/pnas.90.17.7915
  3. Bella JN, 2002, CIRCULATION, V105, P1928, DOI 10.1161/01.CIR.0000015076.37047.D9
  4. Bowden MA, 2015, OBESITY, V23, P1166, DOI 10.1002/oby.21072
  5. Campagnaro BP, 2012, INT J HYPERTENS, DOI 10.1155/2012/968123
  6. Cardillo C, 2002, CIRCULATION, V106, P1783, DOI 10.1161/01.CIR.0000032260.01569.64
  7. COLEMAN DL, 1978, DIABETOLOGIA, V14, P141, DOI 10.1007/BF00429772
  8. da Palma RK, 2016, J APPL PHYSIOL, V121, P1032, DOI 10.1152/japplphysiol.00130.2016
  9. Drel VR, 2006, DIABETES, V55, P3335, DOI 10.2337/db06-0885
  10. DZAU VJ, 1994, CIRCULATION, V89, P493
  11. Fernandez-Real JM, 2003, ENDOCR REV, V24, P278, DOI 10.1210/er.2002-0010
  12. Flues K, 2010, MATURITAS, V65, P267, DOI 10.1016/j.maturitas.2009.11.007
  13. FRIEDMAN JM, 1991, GENOMICS, V11, P1054, DOI 10.1016/0888-7543(91)90032-A
  14. Go AS, 2014, CIRCULATION, V129, pE28, DOI 10.1161/01.cir.0000441139.02102.80
  15. Hasty AH, 2001, J BIOL CHEM, V276, P37402, DOI 10.1074/jbc.M010176200
  16. Heeren MV, 2009, MATURITAS, V62, P200, DOI 10.1016/j.maturitas.2008.12.011
  17. Hilzendeger AM, 2010, J MOL MED-JMM, V88, P383, DOI 10.1007/s00109-009-0569-6
  18. HOTAMISLIGIL GS, 1994, J CLIN INVEST, V94, P1543, DOI 10.1172/JCI117495
  19. IRIGOYEN MC, 1995, HYPERTENSION, V26, P1111
  20. JAMES WPT, 1995, INT J OBESITY, V19, pS37
  21. Janszky I, 2004, J INTERN MED, V256, P421, DOI 10.1111/j.1365-2796.2004.01403.x
  22. JUHANVAGUE I, 1991, DIABETOLOGIA, V34, P457, DOI 10.1007/BF00403280
  23. Kajitani N, 2010, DIABETES RES CLIN PR, V88, P171, DOI 10.1016/j.diabres.2010.01.012
  24. KANNEL WB, 1976, ANN INTERN MED, V85, P447
  25. Kaseta JR, 1999, J CLIN ENDOCR METAB, V84, P1835, DOI 10.1210/jc.84.6.1835
  26. Kiencke S, 2010, EUR J HEART FAIL, V12, P951, DOI 10.1093/eurjhf/hfq110
  27. Kuo TBJ, 2010, ENDOCRINOLOGY, V151, P2613, DOI 10.1210/en.2009-1410
  28. Lau D. C., 2010, PRIM CARE DIABETES, V4, P24, DOI [10.1016/S1751-9918(10)60006-X, DOI 10.1016/S1751-9918(10)60006-X]
  29. Lombardi F, 1996, AM J CARDIOL, V77, P1283, DOI 10.1016/S0002-9149(96)00193-2
  30. Must A, 1999, JAMA-J AM MED ASSOC, V282, P1523, DOI 10.1001/jama.282.16.1523
  31. PINCUS SM, 1991, P NATL ACAD SCI USA, V88, P2297, DOI 10.1073/pnas.88.6.2297
  32. Pinhas-Hamiel O, 2005, J PEDIATR-US, V146, P693, DOI 10.1016/j.jpeds.2004.12.042
  33. Policardo L, 2015, J DIABETES COMPLICAT, V29, P713, DOI 10.1016/j.jdiacomp.2014.12.008
  34. Pradhan AD, 2002, JAMA-J AM MED ASSOC, V288, P980, DOI 10.1001/jama.288.8.980
  35. Raimundo RD, 2013, TRANSL STROKE RES, V4, P488, DOI 10.1007/s12975-013-0263-4
  36. Regitz-Zagrosek V, 2010, CIRC J, V74, P1265, DOI 10.1253/circj.CJ-10-0196
  37. Reichelt ME, 2013, J MOL CELL CARDIOL, V65, P67, DOI 10.1016/j.yjmcc.2013.09.014
  38. Ridker PM, 2000, CIRCULATION, V101, P2149
  39. Ridker PM, 2000, CIRCULATION, V101, P1767
  40. Roncbi FA, 2007, J RENIN-ANGIO-ALDO S, V8, P34, DOI 10.3317/jraas.2007.005
  41. Russo C, 2011, J AM COLL CARDIOL, V57, P1368, DOI 10.1016/j.jacc.2010.10.042
  42. Saleh MC, 2000, BRAIN RES, V879, P105, DOI 10.1016/S0006-8993(00)02757-8
  43. Shimabukuro M, 2011, DIABETES CARE, V34, P686, DOI 10.2337/dc10-1141
  44. Silva SD, 2015, CIRC J, V79, P1372, DOI 10.1253/circj.CJ-14-1179
  45. Srinivasa S, 2015, J CLIN ENDOCR METAB, V100, P2873, DOI 10.1210/jc.2015-1461
  46. Tapsell LC, 2004, DIABETES CARE, V27, P2777, DOI 10.2337/diacare.27.12.2777
  47. Van Gaal LF, 2006, NATURE, V444, P875, DOI 10.1038/nature05487
  48. Verploegen SABW, 1997, FEBS LETT, V405, P237, DOI 10.1016/S0014-5793(97)00192-0
  49. Dantas APV, 2012, EXP DIABETES RES, DOI 10.1155/2012/570598
  50. Wichi R, 2007, CARDIOVASC DIABETOL, V6, DOI 10.1186/1475-2840-6-14
  51. Xue BJ, 2007, AM J PHYSIOL-HEART C, V292, pH1770, DOI 10.1152/ajpheart.01011.2005
  52. ZHANG YY, 1994, NATURE, V372, P425, DOI 10.1038/372425a0