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.

• Main Authors: 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
• Format: Article
• Language: English
• Published: Elsevier 2011-10-01
• Series: Annals of Hepatology
• Subjects: Plasminogen activator inhibitor type 1; Single nucleotide polymorphisms; Liver fibrosis; Non-alcoholic fatty liver disease; Steatosis
• Online Access: http://www.sciencedirect.com/science/article/pii/S1665268119315182

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.