Physical activity levels and hepatic steatosis: A longitudinal follow-up study in adults

Carregando...
Imagem de Miniatura
Citações na Scopus
9
Tipo de produção
article
Data de publicação
2018
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
GERAGE, Aline Mendes
RITTI-DIAS, Raphael Mendes
BALAGOPAL, P. Babu
CONCEICAO, Raquel Dilguerian de Oliveira
UMPIERRE, Daniel
BITTENCOURT, Marcio Sommer
Citação
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, v.33, n.3, p.741-746, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background and AimThis study aimed to evaluate the impact of physical activity (PA) on the course of hepatic steatosis (HS) in adults. MethodsHepatic steatosis status (ultrasonography) and PA levels were evaluated in 5860 subjects at baseline and after approximately 2.5years (range: 19-50months). At follow up, possible exposures to different PA levels were those who remained inactive, became inactive, became active, and remained active. After follow up, subjects were then classified according to the four possible states (outcomes): remained without HS, developed HS (subjects without HS at baseline), remained with HS, or reverted HS. ResultsAfter multivariate adjustments, individuals without HS that became or remained physically active were less likely to develop HS compared with those who remained physically inactive (odds ratio=0.75, P=0.04 and 0.75, P=0.03, respectively). Among those with HS at baseline, becoming and remaining physically active beneficially improved the HS status (odds ratio=0.64, P=0.01 and 0.66, P=0.01, respectively). However, the significance was lost when adjusted for changes in body mass index. ConclusionHigher levels of PA were associated with prevention and treatment of HS, with evidence of effect mediation by changes in body mass index.
Palavras-chave
hepatic steatosis, longitudinal analysis, non-alcoholic fatty liver disease, physical activity
Referências
  1. Ajmera V, 2017, HEPATOLOGY, V65, P65, DOI 10.1002/hep.28776
  2. Alberti KGMM, 2009, CIRCULATION, V120, P1640, DOI 10.1161/CIRCULATIONAHA.109.192644
  3. Baker A, 2016, J OBES, V2016
  4. Brouwers B, 2016, DIABETOLOGIA, V59, P2068, DOI 10.1007/s00125-016-4037-x
  5. Chalasani N, 2012, GASTROENTEROLOGY, V142, P1592, DOI 10.1053/j.gastro.2012.04.001
  6. Craig CL, 2003, MED SCI SPORT EXER, V35, P1381, DOI 10.1249/01.MSS.0000078924.61453.FB
  7. Elias MC, 2010, NUTRITION, V26, P1094, DOI 10.1016/j.nut.2009.09.001
  8. Golabi P, 2016, WORLD J GASTROENTERO, V22, P6318, DOI 10.3748/wjg.v22.i27.6318
  9. Hallsworth K, 2011, GUT, V60, P1278, DOI 10.1136/gut.2011.242073
  10. Hernaez R, 2011, HEPATOLOGY, V54, P1082, DOI 10.1002/hep.24452
  11. Johnson NA, 2009, HEPATOLOGY, V50, P1105, DOI 10.1002/hep.23129
  12. Kwak MS, 2015, LIVER INT, V35, P944, DOI 10.1111/liv.12552
  13. Loomba R, 2009, HEPATOLOGY, V50, P1282, DOI 10.1002/hep.23119
  14. Loria P, 2010, DIGEST LIVER DIS, V42, P272, DOI 10.1016/j.dld.2010.01.021
  15. Meneses-Gaya Carolina de, 2009, Psychol. Neurosci., V2, P83, DOI 10.3922/j.psns.2009.1.12
  16. Musso G, 2011, ANN MED, V43, P617, DOI 10.3109/07853890.2010.518623
  17. Perseghin G, 2007, DIABETES CARE, V30, P683, DOI 10.2337/dc06-2032
  18. Petersen KF, 2005, DIABETES, V54, P603, DOI 10.2337/diabetes.54.3.603
  19. Pickering TG, 2005, CIRCULATION, V111, P697, DOI 10.1161/01.CIR.0000154900.76284.F6
  20. Rohling M, 2016, J DIABETES RES, DOI 10.1155/2016/2868652
  21. Ryu S, 2015, J HEPATOL, V63, P1229, DOI 10.1016/j.jhep.2015.07.010
  22. SCATARIGE JC, 1984, J ULTRAS MED, V3, P9, DOI 10.7863/jum.1984.3.1.9
  23. Shephard RJ, 2015, EUR J APPL PHYSIOL, V115, P1, DOI 10.1007/s00421-014-3031-6
  24. Sung KC, 2016, J HEPATOL, V65, P791, DOI 10.1016/j.jhep.2016.05.026
  25. Vernon G, 2011, ALIMENT PHARM THER, V34, P274, DOI 10.1111/j.1365-2036.2011.04724.x
  26. Younossi ZM, 2016, HEPATOLOGY, V64, P73, DOI 10.1002/hep.28431