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Does non-alcoholic fatty liver impair alterations of plasma lipoproteins and associated factors in metabolic syndrome?

  • Diego Lucero
  • , Valeria Zago
  • , Graciela I. López
  • , Mabel Graffigna
  • , Gustavo H. López
  • , Hugo Fainboim
  • , Verónica Miksztowicz
  • , Leonardo Gómez Rosso
  • , Susana Belli
  • , Oscar Levalle
  • , Gabriela Berg
  • , Fernando Brites
  • , Regina Wikinski
  • , Laura Schreier

Producción científica: Articlerevisión exhaustiva

28 Citas (Scopus)

Resumen

Background: Hepatic steatosis (HS) is closely associated to metabolic syndrome (MS). Both, VLDL-triglyceride oversecretion and intrahepatic deposits, can take place. We evaluated VLDL characteristics, CETP, hepatic lipase (HL), IDL and small dense LDL (sdLDL), in patients with HS associated to MS. Methods: We studied 3 groups matched by age and sex: 25 MS patients with HS (diagnosed by ultrasonography), 25 MS patients without HS and 25 healthy controls. Main measurements were: lipid profile, free fatty acids, VLDL composition, VLDL size by HPLC, CETP and HL activities, IDL-cholesterol and sdLDL-cholesterol. Results: Patients with HS presented higher triglyceride levels, HOMA-IR and free fatty acids, VLDL mass and VLDL-apoB (p < 0.05). No differences in VLDL composition were observed. MS groups presented higher proportion of large VLDL than controls (p < 0.05). HS group showed higher CETP than controls (p = 0.01) and almost higher than MS without HS (p = 0.06). CETP correlated with VLDL-cholesterol content, r = 0.48, p < 0.005. The increase in sdLDL-cholesterol correlated with CETP (r = 0.47) and HL (r = 0.56), independent of insulin resistance (p < 0.003). Conclusion: Despite intrahepatic fat, patients with HS secreted higher number of VLDL particles. CETP would have a remodeling action on VLDL in circulation, enriching it in cholesterol and also favoring, together with HL, the formation of sdLDL.

Idioma originalEnglish
Páginas (desde-hasta)587-592
Número de páginas6
PublicaciónClinica Chimica Acta
Volumen412
N.º7-8
DOI
EstadoPublished - mar 18 2011

Financiación

This study was supported by grants of ANPCyT (Agencia Nacional de Promoción Científica y Tecnologica) , PICT 195 and University of Buenos Aires, B070 .

FinanciadoresNúmero del financiador
Agencia Nacional de Promoción Científica y TecnológicaPICT 195
Universidad de Buenos AiresB070

    ASJC Scopus subject areas

    • Biochemistry
    • Clinical Biochemistry
    • Biochemistry, medical

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