Annals of Hepatology (Oct 2011)

Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease(♦)(♦)This work was supported by grants from the Fondo Nacional de Ciencia y Tecnología de Chile (FONDECYT) #1110455 to M.A., #1100971 to M.A-L. and #1100020 to F.N.

  • Alberto Espino,
  • Andrea Villagrán,
  • Valeska Vollrath,
  • Paulina Hanckes,
  • Roberto Salas,
  • Andrea Farah,
  • Nancy Solís,
  • Margarita Pizarro,
  • Alex Escalona,
  • Camilo Boza,
  • Gustavo Pérez,
  • Gonzalo Carrasco,
  • Oslando Padilla,
  • Juan Francisco Miquel,
  • Flavio Nervi,
  • Norberto C. Chavez-Tapia,
  • Juan Pablo Arab,
  • Manuel Álvarez-Lobos,
  • Marco Arrese,
  • Arnoldo Riquelme

Journal volume & issue
Vol. 10, no. 4
pp. 493 – 501

Abstract

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Background. The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.Aim. To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.Material and methods. Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.Results. BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p < 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).Conclusions. Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fi-brosis in obese patients.

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