BACKGROUND: Genetic variation at the apolipoprotein A-V locus, recently discovered proximal to the APOA1/C3/A4 gene cluster, is associated with elevated triglyceride concentrations, a risk factor for atherosclerosis. METHODS: The goal of our study was to determine the association of two apolipoprotein A-V (APOA5) gene polymorphisms in a group of urban Romanian subjects with the prevalence of the metabolic syndrome. For this purpose, we assayed -1.131T>C and c.56C>G polymorphisms for 279 subjects divided into three groups: a control group, a metabolic syndrome group and a cardiovascular disease group. Then we correlated the minor allele frequencies with body mass index and biochemical parameters. RESULTS: We obtained higher frequency for -1.131C compared to c.56G alleles, both mainly distributed in overweight subjects. Body mass index and triglyceride levels were higher in -1.131C allele carriers in metabolic syndrome patients, but were not significantly different in c.56G carriers compared to those with the native gene. Metabolic syndrome -1.131C homozygotes presented lower high-density lipoprotein cholesterol and higher glucose levels compared to subjects with the native gene. Total cholesterol, low-density lipoprotein cholesterol and insulin were not different between -1.131C or c.56G allele carriers and those with the native gene. CONCLUSIONS: Our results demonstrate an independent risk for -1.131T>C APOA5 gene polymorphisms in the development of metabolic syndrome.
BACKGROUND: Genetic variation at the apolipoprotein A-V locus, recently discovered proximal to the APOA1/C3/A4 gene cluster, is associated with elevated triglyceride concentrations, a risk factor for atherosclerosis. METHODS: The goal of our study was to determine the association of two apolipoprotein A-V (APOA5) gene polymorphisms in a group of urban Romanian subjects with the prevalence of the metabolic syndrome. For this purpose, we assayed -1.131T>C and c.56C>G polymorphisms for 279 subjects divided into three groups: a control group, a metabolic syndrome group and a cardiovascular disease group. Then we correlated the minor allele frequencies with body mass index and biochemical parameters. RESULTS: We obtained higher frequency for -1.131C compared to c.56G alleles, both mainly distributed in overweight subjects. Body mass index and triglyceride levels were higher in -1.131C allele carriers in metabolic syndromepatients, but were not significantly different in c.56G carriers compared to those with the native gene. Metabolic syndrome -1.131C homozygotes presented lower high-density lipoprotein cholesterol and higher glucose levels compared to subjects with the native gene. Total cholesterol, low-density lipoprotein cholesterol and insulin were not different between -1.131C or c.56G allele carriers and those with the native gene. CONCLUSIONS: Our results demonstrate an independent risk for -1.131T>C APOA5 gene polymorphisms in the development of metabolic syndrome.
Authors: Eva Gesteiro; Sara Bastida; Miguel Vázquez-Velasco; Dolores Corella; Marisa Guillén; Jose M Ordovas; Francisco J Sánchez-Muniz Journal: Eur J Pediatr Date: 2011-04-20 Impact factor: 3.183
Authors: Mary F Feitosa; Ping An; Jose M Ordovas; Shamika Ketkar; Paul N Hopkins; Robert J Straka; Donna K Arnett; Ingrid B Borecki Journal: Atherosclerosis Date: 2011-01-21 Impact factor: 5.162
Authors: Stefan K Nilsson; Stine Christensen; Merete K Raarup; Robert O Ryan; Morten S Nielsen; Gunilla Olivecrona Journal: J Biol Chem Date: 2008-07-03 Impact factor: 5.157