Plasma kinetics of an LDL-like nanoemulsion and lipid transfer to HDL in subjects with glucose intolerance

Imagem de Miniatura
Arquivos
art_BERTATO_Plasma_kinetics_of_an_LDL_like_nanoemulsion_and_2012.PDF (272.76 KB)
Citações na Scopus
9
Tipo de produção
article
Data de publicação
2012
DOI
SciELO
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
HOSPITAL CLINICAS, UNIV SAO PAULO
Autores
Citação
CLINICS, v.67, n.4, p.347-353, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
OBJECTIVE: Glucose intolerance is frequently associated with an altered plasma lipid profile and increased cardiovascular disease risk. Nonetheless, lipid metabolism is scarcely studied in normolipidemic glucose-intolerant patients. The aim of this study was to investigate whether important lipid metabolic parameters, such as the kinetics of LDL free and esterified cholesterol and the transfer of lipids to HDL, are altered in glucose-intolerant patients with normal plasma lipids. METHODS: Fourteen glucose-intolerant patients and 15 control patients were studied; none of the patients had cardiovascular disease manifestations, and they were paired for age, sex, race and co-morbidities. A nanoemulsion resembling a LDL lipid composition (LDE) labeled with C-14-cholesteryl ester and H-3-free cholesterol was intravenously injected, and blood samples were collected over a 24-h period to determine the fractional clearance rate of the labels by compartmental analysis. The transfer of free and esterified cholesterol, triglycerides and phospholipids from the LDE to HDL was measured by the incubation of the LDE with plasma and radioactivity counting of the supernatant after chemical precipitation of non-HDL fractions. RESULTS: The levels of LDL, non-HDL and HDL cholesterol, triglycerides, apo A1 and apo B were equal in both groups. The 14 C-esterified cholesterol fractional clearance rate was not different between glucose-intolerant and control patients, but the H-3-free- cholesterol fractional clearance rate was greater in glucose-intolerant patients than in control patients. The lipid transfer to HDL was equal in both groups. CONCLUSION: In these glucose-intolerant patients with normal plasma lipids, a faster removal of LDE free cholesterol was the only lipid metabolic alteration detected in our study. This finding suggests that the dissociation of free cholesterol from lipoprotein particles occurs in normolipidemic glucose intolerance and may participate in atherogenic signaling.
Palavras-chave
Cholesterol, Emulsions, Nanoparticles, Lipoproteins
URI
https://observatorio.fm.usp.br/handle/OPI/457
Referências
  1. Ades A, 2001, GYNECOL ONCOL, V82, P84, DOI 10.1006/gyno.2001.6203
  2. American Diabetes Association (ADA), 2008, DIABETES CARE S1, V31, pS55
  3. Assmann G, 2004, CIRCULATION, V109, P8, DOI 10.1161/01.CIR.0000131512.50667.46
  4. Azevedo CHM, 2011, CLINICS, V66, P1543, DOI 10.1590/S1807-59322011000900006
  5. Chan DC, 2002, METABOLISM, V51, P1041, DOI 10.1053/meta.2002.33339
  6. Chan DC, 2005, CLIN BIOCHEM, V38, P806, DOI 10.1016/j.clinbiochem.2005.05.009
  7. Couto RD, 2007, LIPIDS, V42, P411, DOI 10.1007/s11745-007-3041-9
  8. Dantas SA, 2010, CLINICS, V65, P23, DOI 10.1590/S1807-59322010000100005
  9. Dobiasova M, 1998, PHYSIOL RES, V47, P387
  10. Ginsberg HN, 2000, J CARDIOVASC RISK, V7, P325
  11. Gylling H, 1997, DIABETES CARE, V20, P90, DOI 10.2337/diacare.20.1.90
  12. Hirata RDC, 1999, BBA-MOL CELL BIOL L, V1437, P53, DOI 10.1016/S1388-1981(98)00004-3
  13. Hungria VTM, 2004, CANCER CHEMOTH PHARM, V53, P51, DOI 10.1007/s00280-003-0692-y
  14. Julius U, 2007, INT J CLIN PRACT, V61, P1798, DOI 10.1111/j.1742-1241.2007.01507.x
  15. KISSEBAH AH, 1987, DIABETES METAB REV, V3, P619
  16. Lo Prete AC, 2009, LIPIDS, V44, P917, DOI 10.1007/s11745-009-3342-2
  17. Maranhao RC, 2012, CLIN CHIM ACTA, V413, P502, DOI 10.1016/j.cca.2011.11.011
  18. MARANHAO RC, 1993, LIPIDS, V28, P691, DOI 10.1007/BF02535988
  19. MARANHAO RC, 1994, CANCER RES, V54, P4660
  20. Maranhao RC, 1997, LIPIDS, V32, P627, DOI 10.1007/s11745-997-0080-6
  21. Masson D, 2009, J LIPID RES S, pS201
  22. Mesquita CH, 1994, CINETICA LDL MARCADA
  23. Nagaretani H, 2001, DIABETES CARE, V24, P2127, DOI 10.2337/diacare.24.12.2127
  24. Novoa FJ, 2005, DIABETES CARE, V28, P2388, DOI 10.2337/diacare.28.10.2388
  25. Parhofer KG, 2006, J LIPID RES, V47, P1620, DOI 10.1194/jlr.R600013-JLR200
  26. Pietzsch J, 2003, CROAT MED J, V44, P171
  27. Pietzsch J, 1999, ANN NY ACAD SCI, V892, P323, DOI 10.1111/j.1749-6632.1999.tb07808.x
  28. Pont F, 2002, ARTERIOSCL THROM VAS, V22, P1726, DOI 10.1161/01.ATV.0000032134.92180.41
  29. Riches FM, 1998, INT J OBESITY, V22, P414, DOI 10.1038/sj.ijo.0800602
  30. Santos RD, 2003, J LIPID RES, V44, P464, DOI 10.1194/jlr.M200331-JLR200
  31. Saydah SH, 2001, DIABETES CARE, V24, P447, DOI 10.2337/diacare.24.3.447
  32. Sowby FS, 1984, ICRP PUBLICATION 1
  33. STERN MP, 1995, DIABETES, V44, P369, DOI 10.2337/diabetes.44.4.369
  34. Taskinen MR, 2002, ATHEROSCLEROSIS SUPP, V3, P47, DOI 10.1016/S1567-5688(01)00006-X
  35. The DECODE Study Group the European Diabetes Epidemiology Group, 2001, ANN INTERN MED, V61, P397
  36. The Oxford Center for Diabetes Endocrinology e Metabolism, HOMA CALC
  37. WAJCHENBERG BL, 1995, J CLIN ENDOCR METAB, V80, P2791, DOI 10.1210/jc.80.9.2791
  38. Watanabe N, 1999, DIABETES CARE, V22, P152, DOI 10.2337/diacare.22.1.152

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/18
Artigos e Materiais de Revistas Científicas - LIM/31