Phytosterol containing diet increases plasma and whole body concentration of phytosterols in apoE-KO but not in LDLR-KO mice

Imagem de Miniatura
Arquivos
art_NUNES_Phytosterol_containing_diet_increases_plasma_and_whole_body_2019.PDF (412.97 KB)
Citações na Scopus
5
Tipo de produção
article
Data de publicação
2019
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER/PLENUM PUBLISHERS
Autores
Citação
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, v.51, n.2, p.131-136, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Phytosterol metabolism is unknown in the hypercholesterolemia of genetic origin. We investigated the metabolism of phytosterols in a cholesterol-free, phytosterol-containing standard diet in hypercholesterolemic mice knockouts for low density lipoprotein receptor (LDLR) and apolipoprotein E (apoE) mice compared to wild-type mice (controls). Phytosterols were measured in mice tissues by GCMS. ApoE-KO mice absorbed less phytosterols than LDLR-KO and the latter absorbed less phytosterols than control mice, because the intestinal campesterol content was low in both KO mice, and sitosterol was low in the intestine in apoE-KO mice as compared to LDLR-KO mice. Although the diet contained nine times more sitosterol than campesterol, the concentration of sitosterol was lower than that of campesterol in plasma in LDLR-KO, and in the liver in controls and in LDLR-KO, but only in apoE-KO. On the other hand, in the intestine sitosterol was higher than campesterol in controls, and in LDLR-KO but with a tendency only in apoE-KO. Because of the high dietary supply of sitosterol, sitosterol was better taken up by the intestine than campesterol, but the amount of sitosterol was lower than that of campesterol in the liver, while in the whole body the amounts of these phytosterols do not differ from each other. Therefore, via intestinal lymph less sitosterol than campesterol was transferred to the body. However, as compared to controls, in apoE-KO mice, but not in LDLR-KO mice, the increase in campesterol and sitosterol in plasma and in the whole body indicating that apoE-KO mice have a marked defect in the elimination of both phytosterols from the body.
Palavras-chave
Knockout mice, Phytosterols, Hypercholesterolemia, Apo E knockout mice, Low density lipoprotein receptor
URI
https://observatorio.fm.usp.br/handle/OPI/31595
Referências
  1. Andersson SW, 2004, EUR J CLIN NUTR, V58, P1378, DOI 10.1038/sj.ejcn.1601980
  2. Baila-Rueda L, 2016, ATHEROSCLEROSIS, V246, P202, DOI 10.1016/j.atherosclerosis.2016.01.005
  3. BHATTACHARYYA AK, 1981, AM J PHYSIOL, V240, pG50
  4. Bombo RPA, 2013, ATHEROSCLEROSIS, V231, P442, DOI 10.1016/j.atherosclerosis.2013.10.015
  5. Calandra S, 2017, CURR OPIN LIPIDOL, V28, P267, DOI 10.1097/MOL.0000000000000414
  6. GRUNDY SM, 1969, J LIPID RES, V10, P304
  7. Gylling H, 2005, ANN CLIN BIOCHEM, V42, P254, DOI 10.1258/0004563054255605
  8. Gylling H, 2014, ATHEROSCLEROSIS, V232, P346, DOI 10.1016/j.atherosclerosis.2013.11.043
  9. Hamada T, 2006, LIPIDS, V41, P551, DOI 10.1007/s11745-006-5004-y
  10. Kohler J, 2017, BRIT J PHARMACOL, V174, P1281, DOI 10.1111/bph.13764
  11. Lupattelli G, 2012, NUTR METAB CARDIOVAS, V22, P231, DOI 10.1016/j.numecd.2010.05.010
  12. Martins CM, 2013, NUTRITION, V29, P865, DOI 10.1016/j.nut.2012.12.017
  13. Matthan NR, 2009, J LIPID RES, V50, P1927, DOI 10.1194/jlr.P900039-JLR200
  14. Miettinen TA, 2011, NUTR METAB CARDIOVAS, V21, P765, DOI 10.1016/j.numecd.2011.05.005
  15. Miettinen TA, 2006, GASTROENTEROLOGY, V130, P542, DOI 10.1053/j.gastro.2005.10.022
  16. Moghadasian MH, 2001, METABOLISM, V50, P708, DOI 10.1053/meta.2001.23303
  17. Moruisi KG, 2006, J AM COLL NUTR, V25, P41, DOI 10.1080/07315724.2006.10719513
  18. Mymin D, 2018, ATHEROSCLEROSIS, V269, P122, DOI 10.1016/j.atherosclerosis.2017.12.024
  19. National Research Council, 2011, GUIDE CARE USE LAB A, DOI [10. 17226/12910, DOI 10.17226/12910, 10.17226/12910]
  20. Nunes VS, 2011, CLIN CHIM ACTA, V412, P176, DOI 10.1016/j.cca.2010.09.039
  21. Nunes VS, 2018, J BIOENERG BIOMEMBR, V50, P283, DOI 10.1007/s10863-018-9757-9
  22. Ooi EMM, 2010, J LIPID RES, V51, P2413, DOI 10.1194/jlr.M004705
  23. OSONO Y, 1995, J CLIN INVEST, V95, P1124, DOI 10.1172/JCI117760
  24. Plat J, 2008, METABOLISM, V57, P1241, DOI 10.1016/j.metabol.2008.04.018
  25. Rysz J, 2017, CURR PHARM DESIGN, V23, P2488, DOI 10.2174/1381612823666170316112344
  26. SAMUEL P, 1983, J LIPID RES, V24, P265
  27. Simonen P, 2008, ATHEROSCLEROSIS, V197, P883, DOI 10.1016/j.atherosclerosis.2007.08.003
  28. Sioen I, 2011, BRIT J NUTR, V105, P960, DOI 10.1017/S0007114510004587
  29. Stellaard F, 2017, J STEROID BIOCHEM, V169, P111, DOI 10.1016/j.jsbmb.2016.03.030
  30. Tang WQ, 2009, J LIPID RES, V50, P293, DOI 10.1194/jlr.M800439-JLR200
  31. von Bergmann K, 2005, AM J CARDIOL, V96, p10D, DOI 10.1016/j.amjcard.2005.03.014
  32. Wang J, 2015, J LIPID RES, V56, P319, DOI 10.1194/jlr.M054544
  33. Weingartner O, 2015, J AOAC INT, V98, P742, DOI 10.5740/jaoacint.SGEWeingartner
  34. Woollett LA, 1995, P NATL ACAD SCI USA, V92, P12500, DOI 10.1073/pnas.92.26.12500

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - LIM/10