Adiposidade corporal, mas não resistência insulínica, associa-se ao polimorfismo -675 4G/5G no gene PAI-1 em uma amostra de crianças mexicanas / Body adiposity but not insulin resistance is associated with -675 4G/5G polymorphism in the PAI-1 gene in a sample of Mexican children

OBJETIVO: Elaboramos este estudo para avaliar se o polimorfismo -675 4G/5G no gene inibidor 1 do ativador do plasminogênio se associa à obesidade e à resistência insulínica em crianças mexicanas. MÉTODOS: Foi realizado um estudo transversal em 174 crianças, 89 delas com peso normal e 85 obesas, variando sua idade de 6 a 13 anos. Todas as crianças eram do estado de Guerrero e foram recrutadas de três escolas primárias na cidade de Chilpancingo, México. Os níveis de insulina foram determinados por prova imunoenzimática. Foi usado o modelo de avaliação da homeostase para determinar resistência insulínica. O polimorfismo -675 4G/5G no gene PAI-1 foi analisado pelo método reação de polimerase em cadeia-polimorfismo no comprimento dos fragmentos de restrição. RESULTADOS: A prevalência de resistência insulínica no grupo obeso foi mais alta (49,41%) do que no grupo com peso normal (16,85%). O polimorfismo 4G/5G do PAI-1 foi encontrado em equilíbrio de Hardy Weinberg. O genótipo 4G/5G contribuiu para um aumento significativo da relação cintura-quadril (β = 0,02, p = 0,006), da circunferência da cintura (β = 4,42, p = 0,009) e da espessura da prega subescapular (β = 1,79, p = 0,04), mas não se relacionou com a resistência insulínica. CONCLUSÃO: O genótipo -675 4G/5G do gene PAI-1 se associou a aumento da adiposidade corporal em crianças mexicanas.

OBJECTIVE: To assess whether the -675 4G/5G polymorphism in the plasminogen activator inhibitor-1 gene is associated with obesity and insulin resistance in Mexican children. METHODS: A cross-sectional study was performed in 174 children, 89 with normal-weight and 85 with obesity, aged from 6 to 13 years. All children were from state of Guerrero, and recruited from three primary schools in the city of Chilpancingo, Mexico. Insulin levels were determined by immunoenzymatic assay. The homeostasis model assessment was used to determine insulin resistance. The -675 4G/5G polymorphism in PAI-1 gene was analyzed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The prevalence of insulin resistance in the obese group was higher (49.41%) than in the normal-weight group (16.85%). The 4G/5G PAI-1 polymorphism was found in Hardy Weinberg equilibrium. The 4G/5G genotype contributed to a significant increase in waist-hip ratio (β = 0.02, p = 0.006), waist circumference (β = 4.42, p = 0.009), and subscapular skinfold thickness (β = 1.79, p = 0.04); however, it was not related with insulin resistance. CONCLUSION: The -675 4G/5G genotype of PAI-1 gene was associated with increase of body adiposity in Mexican children.

Relationship between plasminogen activator inhibitor type-1 (PAI-1) gene polymorphisms and osteoporosis in Turkish women

OBJECTIVE: The development of osteoporosis is associated with several risk factors, such as genetic structures that affect bone turnover and bone mass. The impact of genetic structures on osteoporosis is not known. Plasminogen activator inhibitor type-1 regulates the bone matrix and bone balance. This study assessed the correlation between plasminogen activator inhibitor type-1 gene 4G/5G polymorphisms and osteoporosis in a population of Turkish women. METHODS: A total of 195 postmenopausal female patients who were diagnosed with osteoporosis (Group I) based on bone mineral density measurements via dual-energy x-ray absorptiometry and 90 females with no osteoporosis (Group II) were included in this study. Correlations between PAI-1 gene 4G/5G polymorphisms and osteoporosis were investigated through the identification of PAI-1 gene 4G/5G polymorphism genotypes using the polymerase chain reaction. RESULTS: No significant differences in the genotype and allele frequency of 4G/5G plasminogen activator inhibitor type-1 polymorphisms were observed between the two groups, and both groups exhibited the most frequently observed 4G5G genotype. CONCLUSION: No correlation between the development of osteoporosis in the female Turkish population and 4G/5G plasminogen activator inhibitor type-1 gene polymorphisms was observed.

The association of PAI-1 gene polymorphism with cerebral infarction and recurrent cerebral infarction / 临床神经病学杂志

Objective To investigate the association of the gene polymorphism of plasminogen activator inhibitor 1 (PAI 1) with the cerebral infarction and recurrent cerebral infarction (RCI). Methods The plasma PAI 1 activity, by means of chromgenic substrate assay, and the sequence polymorphisms of 4G/5G in promotor region and (CA)n dinucleotide repeats in the 4th intron of PAI 1 gene, by amplified fragment length polymorphism assay, were measured in 50 patients with first ever cerebral infarction (FCI), 45 patients with RCI and 60 healthy controls.Results The plasma PAI 1 activities in both FCI patients (1.13?1 1 AU/ml) and RCI (1.13?0.150 AU/ml) were remarkably higher than that in the controls (0.7?0.25 AU/ml) (both P

PPAR-? ligand in suppressing radiation induced PAI-1 upregulation / 中华放射肿瘤学杂志

Objective observe the post-radiation expression of rat mesangial cell plasminogen activator inhibitor-1 (PAI-1), and the effect of PPAR-? ligand on radiation induced PAI-1 expression. Methods After 10?Gy ?-ray radiation of cultured rat kidney mesangial cell, RT-PCR was used to observe PPAR-?expression. PAI-1 expression after 10?Gy radiation ?10?mmol/L pioglitazone (one of PPAR-? ligands) was measured by Northern blot and Western blot. Gel-shift method was used to study the effect of AP-1 of PPAR-? ligand on radiation induced PAI-1 expression. Methods Rat kidney mesangial cell expressed PPAR--? mRNA. PAI-1 over-expressed at 24 hour after 10?Gy radiation in a radiation dose dependent manner, but not at other time. When the cell was treated with 10?Gy + 10?mmol/L pioglitazone, PAI-1 upregulation was blunted at message and protein level. AP-1 activation was increased from the 2nd hour after 10?Gy radiation and reached the highest level at the 4th hour. When pioglitazone was added, the radiation induced increase in AP-1 activation was suppressed at the 4th hour. Conclusions Pioglitazone, mediated by AP-1 gene, can suppress radiation induced PAI-1 upregulation.