Ir para o conteúdo principal Ir para o menu de navegação principal Ir para o rodapé
Scientific Electronic Archives
Ciências da Saúde
DOI: 10.36560/14820211433
Enviado: 2021-07-07
Publicado: 2021-07-30

Obesity progression causes liver steatosis and co-morbidities without apparent cardiac metabolic and functional decline

Universidade Federal de Mato Grosso, Campus Sinop
Faculdade de Medicina de Botucatu - UNESP
Faculdade de Medicina de Botucatu - UNESP
Faculdade de Medicina de Botucatu - UNESP
Faculdade de Medicina de Botucatu - UNESP
Faculdade de Medicina de Botucatu - UNESP
Universidade Federal de Mato Grosso, Campus Sinop
Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University
Departamento de Clínica Médica – Faculdade de Medicina de Botucatu

Resumo

The goal of this study was to test if obesity progression can be a risk factor to alter cardiac metabolism and function along the time. Male Wistar rats were randomly divided to receive either chow diet (12.0% calories from fat) [C group] or high-fat diet (49.7% calories from fat) plus sucrose in the drinking water (100% from carbohydrate) [H group] for 6, 12 and 24 weeks. The Western diet significantly increased adiposity index of rats in all three experimental periods compared to C group. This was associated with increased plasma levels of insulin, resistin, leptin, glucose, triacylglycerol and decreased adiponectin, however, all variables were stable along the time except insulin and leptin. Plasma free fatty acid was only elevated with 24 weeks treatment. The obesity status resulted in hepatic steatosis progression in H group, while oxidative stress, hepatic inflammatory foci as well as TNF-α and IL-6 mRNA levels were not affected. There are no cardiac performance decline as well as metabolism cardiac changes in H group when compared with C. In conclusion, Western diet induced and promoted obesity, co-morbidities and hepatic steatosis progression while was not associated with apparent alterations of cardiac metabolism and function. These results suggest that obesity progression seems to affect the organs of distinct ways, and cardiac dysfunction is a question of time

Referências

  1. ALEXANDER, J.K., ALPERT, M.A. Hemodynamic alterations with obesity in man. In: Alpert M.A., Alexander J.K (eds). The heart and lung in obesity: Armonk, NY: Futura Publishing Company 1998; 45-55.
  2. ALPERT, M.A, OMRAN, J., BOSTICK, B.P. Effects of Obesity on Cardiovascular Hemodynamics, Cardiac Morphology, and Ventricular Function. Curr Obes Rep 5(4):424-434, 2016. doi: 10.1007/s13679-016-0235-6
  3. ALPERT, M.A., KARTHIKEYAN, K., ABDULLAH, O., GHADBAN, R. Obesity and Cardiac Remodeling in Adults: Mechanisms and Clinical Implications. Prog Cardiovasc Dis 61(2):114-123, 2018. doi: 10.1016/j.pcad.2018.07.012
  4. ANGULO P. Nonalcoholic fatty liver disease. N Engl J Med 346(16):1221-1231, 2002. doi: 10.1056/NEJMra011775.
  5. BONCI, E., CHIESA, C., VERSACCI, P., ANANIA, C., SILVESTRI, L., PACIFICO L. Association of Nonalcoholic Fatty Liver Disease with Subclinical Cardiovascular Changes: A Systematic Review and Meta-Analysis. Biomed Res Int 2015:213737, 2015. doi: 10.1155/2015/213737
  6. BORGES-CANHA, M., NEVES, J.S., LIBÂNIO, D., VON-HAFE, M., VALE, C., ARAUJO-MARTINS, M., et al. Association between nonalcoholic fatty liver disease and cardiac function and structure-a meta-analysis. Endocrine 66(3):467-476, 2019. doi: 10.1007/s12020-019-02070-0
  7. CAROBBIO, S., PELLEGRINELLI, V., VIDAL-PUIG, A. Adipose Tissue Function and Expandability as Determinants of Lipotoxicity and the Metabolic Syndrome. Adv Exp Med Biol 960:161-196, 2017. doi: 10.1007/978-3-319-48382-5_7.
  8. CLARK, J.M., BRANCATI, F.L., DIEHL, A.M. Nonalcoholic fatty liver disease. Gastroenterology 122(6):1649-1657, 2002. doi: 10.1053/gast.2002.33573
  9. D'SOUZA, K., NZIRORERA, C., KIENESBERGER, P.C. Lipid metabolism and signaling in cardiac lipotoxicity. Biochim Biophys Acta 1861(10):1513-1524, 2016. doi: 10.1016/j.bbalip.2016.02.016
  10. FRANCISQUETI, F.V., NASCIMENTO, A.F., MINATEL, I.O., DIAS, M.C., LUVIZOTTO, R.A.M., BARCHIERI-RONCHI, C., et al. Metabolic syndrome and inflammation in adipose tissue occur at different times in animals submitted to a high-sugar/fat diet. J Nutr Sci 6:e41, 2017. doi:10.1017/jns.2017.42
  11. GHABEN, A.L., SCHERER, P.E. Adipogenesis and metabolic health. Nat Rev Mol Cell Biol 20(4):242-258, 2019. doi: 10.1038/s41580-018-0093-z.
  12. KENCHAIAH, S., EVANS, J.C., LEVY, D., WILSON, P.W.F., BENJAMIN, E.J., LARSON, M.G., et al. Obesity and the risk ofheart failure. N Engl J Med 347:305–313, 2002. doi: 10.1056/NEJMoa020245
  13. LOEHR, L.R., ROSAMOND, W.D., POOLE, C., MCNEILL, A.M., CHANG, P.P., FOLSOM, A.R., et al. Association ofmultiple anthropometrics of overweight and obesity withincident heart failure: the Atherosclerosis Risk in Comm u-nities Study. Circ Heart Fail 2:18–24, 2009. doi: 10.1161/CIRCHEARTFAILURE.108.813782
  14. LOPASCHUK, G.D., FOLMES, C.D., STANLEY, W.C. Cardiac energy metabolism in obesity. Circ Res 101(4):335-347, 2007. doi: 10.1161/CIRCRESAHA.107.150417
  15. LUVIZOTTO RAM, NASCIMENTO AF, IMAIZUMI E, PIERINE, D.T., CONDE, S.J., CORREA, C.R., et al. Lycopene supplementation modulates plasma concentration and epididymal adipose tissue mRNA of leptin, resistin and IL-6 in diet-induced obese rats. Br J Nutr 110(10):1803-1809, 2013. doi: 10.1017/S0007114513001256
  16. MARRA, F., SVEGLIATI-BARONI, G. Lipotoxicity and the gut-liver axis in NASH pathogenesis. J Hepatol 68(2):280-295, 2018. doi: 10.1016/j.jhep.2017.11.014
  17. NASCIMENTO AF, LUVIZOTTO RAM, LEOPOLDO AS, LIMA-LEOPOLDO, A.P., SEIVA, F.R., JUSTULIN JR, L.A., et al. Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity. Life Science 88:1031-1038, 2011. doi: 10.1016/j.lfs.2011.03.015
  18. NISHI, H., HIGASHIHARA, T., INAGI, R. Lipotoxicity in Kidney, Heart, and Skeletal Muscle Dysfunction. Nutrients 11(7):1664, 2019. doi: 10.3390/nu11071664
  19. NOVELLI, E.L., SOUZA, G.A., EBAID, G.M., ROCHA, K.K.H.R., SEIVA, F.R.F., MANI, F., et al. Energy expenditure and oxygen consumption as novel biomarkers of obesity-induced cardiac disease in rats. Obesity (Silver Spring) 18(9):1754-1761, 2010. doi: 10.1038/oby.2009.470
  20. RONCHI, C.F., FIORETTO, J.R., FERREIRA, A.L., BERCHIERI-RONCHI, C. B., CORREA, C.R., KUROKAWA, C.S., et al. Biomarkers for oxidative stress in acute lung injury induced in rabbits submitted to different strategies of mechanical ventilation. J Appl Physiol 112:1184-1190, 2012. doi: 10.1152/japplphysiol.01334.2011
  21. SLETTEN, A.C., PETERSON, L.R., SCHAFFER, J.E. Manifestations and mechanisms of myocardial lipotoxicity in obesity. J Intern Med 284(5):478-491, 2018. doi: 10.1111/joim.12728
  22. SLETTEN, A.C., PETERSON, L.R., SCHAFFER, J.E. Manifestations and mechanisms of myocardial lipotoxicity in obesity. J Intern Med 284(5):478-491, 2018. doi: 10.1111/joim.12728
  23. WANG, Y., SEITZ, H.K., WANG, X.D. Moderate alcohol consumption aggravates high-fat diet induced steatohepatitis in rats. Alcohol Clin Exp Res 34:567-573, 2010. doi: 10.1111/j.1530-0277.2009.01122.x
  24. WENDE, A.R., ABEL, E.D. Lipotoxicity in the heart. Biochim Biophys Acta 1801(3):311-319, 2010. doi: 10.1016/j.bbalip.2009.09.023.

Como Citar

Nascimento, A. F. do ., Martins, A. de O. ., Oliveira, T. A. S. de ., Correa, C. R. ., Okoshi, K. ., Ferreira, A. L. dos A. ., … Cicogna, A. C. (2021). Obesity progression causes liver steatosis and co-morbidities without apparent cardiac metabolic and functional decline. Scientific Electronic Archives, 14(8). https://doi.org/10.36560/14820211433