Association of uricemia with biochemical and dietary factors in human adults with metabolic syndrome genotyped to C677T polymorphism in the methylenetetrahydrofolate reductase gene.

It is suggested that hyperuricemia is a marker of cardiovascular risk in human adults with metabolic syndrome (MS). The C677T polymorphism in the gene encoding the enzyme methylenetetrahydrofolate reductase (MTHFR) is associated with hyperuricemia. Data on factors associated with uricemia in human adults with MS genotyped for this polymorphism are lacking. We aimed to investigate the factors associated with uricemia in human adults with MS genotyped for the C677T polymorphism in the MTHFR gene. Cross-sectional study was conducted with 63 human adults (24 men and 39 women) with MS. Body weight, body mass index, waist circumference, body fat, glycemia, lipid profile, uricemia, insulinemia, homocysteinemia, plasma folate, erythrocyte folate, blood pressure, smoking, diuretics use, usual dietary alcohol and protein intakes, MTHFR and the presence of the C677T polymorphism in the gene were assessed. Hyperuricemia was observed in 16 (25.4%) human adults (10 men and 6 women). In the group, 33% (n = 21) showed the C677T polymorphism, being 19 heterozygous and 2 mutant homozygous. A significant association between hyperuricemia and C677T polymorphism was not verified. Uricemia was positively associated with homocys-teinemia (r = 0.43, p < 0.05), triglyceridemia (r = 0.41, p<0.05), serum concentrations of very-low-density lipoprotein (r = 0.27, p< 0.05) and the habitual alcohol intake (r = 0.37, p < 0.05). However, only homocysteinemia, triglyc-eridemia, and habitual alcohol intake remained in the final model of linear regression. In human adults with MS geno-typed for the C677T polymorphism in the MTHFR gene, uricemia was positively associated with homocysteinemia, triglyceridemia and the habitual alcohol intake.

Association of uricemia with biochemical and dietary factors in human adults with metabolic syndrome genotyped to C677T polymorphismin the methylenetetrahydrofolate reductase gene / Asociación de la uricemia con factores bioquímicos y dietéticos en humanos adultos con síndrome metabólico genotipados para el polimorfismo C677T en el gen metilenotetrahidrofolato reductasa

It is suggested that hyperuricemia is a marker of cardiovascular risk in human adults with metabolic syndrome(MS). The C677T polymorphism in the gene encoding the enzyme methylenetetrahydrofolate reductase (MTHFR) is associated with hyperuricemia. Data on factors associated with uricemia in human adults with MS genotyped for this polymorphism are lacking. We aimed to investigate the factors associated with uricemia in human adults with MSgenotyped for the C677T polymorphism in the MTHFR gene. Cross-sectional study was conducted with 63 human adults (24 men and 39 women) with MS. Body weight, body mass index, waist circumference, body fat, glycemia, lipidprofile, uricemia, insulinemia, homocysteinemia, plasmafolate, erythrocyte folate, blood pressure, smoking, diuretics use, usual dietary alcohol and protein intakes, and the presence of the C677T polymorphism in the MTHFR gene were assessed. Hyperuricemia was observed in 16 (25.4%)human adults (10 men and 6 women). In the group, 33% (n= 21) showed the C677T polymorphism, being 19 heterozygous and 2 mutant homozygous. A significant association between hyperuricemia and C677T polymorphism was not verified. Uricemia was positively associated with homocysteinemia (r = 0.43, p < 0.05), triglyceridemia (r = 0.41,p<0.05), serum concentrations of very-low-density lipoprotein(r = 0.27, p< 0.05) and the habitual alcohol intake (r =0.37, p < 0.05). However, only homocysteinemia, triglyceridemia, and habitual alcohol intake remained in the final model of linear regression. In human adults with MS genotyped for the C677T polymorphism in the MTHFR gene, uricemia was positively associated with homocysteinemia, triglyceridemia and the habitual alcohol intake (AU)

Sugiérese que la hiperuricema sea un factor de riesgo cardiovascular en humanos adultos con síndrome metabólico(SM) El polimorfismo C677T en el gen metilenotetrahidrofolato reductasa (MTHFR) ha sido asociado com la hiperuricemia. Datos sobre los factores asociados con la uricemia en humanos adultos con SM genotipados para el polimorfismo C677T en el gen MTHFR son inexistentes. Se objetivó investigar los factores asociados con lauricemia en individuos con SM genotipados para el polimorfismo C677T. Se ha realizado un estudio transversal con 63 humanos adultos (24 hombres y 39 mujeres). Fueron evaluados peso, altura, índice de masa corporal, circunferencia de la cintura, grasa corporal total, glucemia, uricemia, insulinemia, homocisteinemia, folato plasmático, folato en los eritrocitos, presión arterial, tabaquismo,uso de diuréticos, ingesta habitual de proteínas dietéticas y de alcohol y la presencia del polimorfismo C677T. No fue encontrado asociación significativa entre el polimorfismo C677T y la uricemia. Fue verificado que un 25,4% (n = 16) do los individuos presentaban hiperuricemia (10 hombres y 6 mujeres). Se verificó que un 33%(n = 21) de los individuos presentaron el polimorfismo C677T (19 heterocigotos y 2 homocigotos polimórficos). La uricemia se asoció con los niveles de homocisteina (r =0,43, p < 0,05), trigicéridos (r = 0,41, p < 0,05) y de lipoproteínas de muy baja densidad (r = 0.27, p < 0,05) y conla ingesta de alcohol (r = 0,37, p < 0,05). Sin embargo, sólo la homocisteinemia, la trigliceridemia y la ingesta habitual de alcohol permanecerán en el modelo final de regresión lineal. En los humanos adultos con SM genotipados para el polimorfismo C677T en el gen MTHFR, la uricemia se asoció positivamente con los niveles de homocisteína y triglicéridos y con la ingesta habitual de alcohol (AU)

[Influence of fat diet in glicidic metabolism in obese women with Pro12Pro genotype in PPARgamma2 gene]. / Influencia de la grasa de la dieta en el metabolismo glucídico de mujeres obesas con el genotipo Pro12Pro en el gen PPARgama2.

INTRODUCTION: The peroxisome proliferator-activated receptor gamma 2 (PPARgamma2) is an adipogenic transcription factor that influences in insulin resistance (IR) in the presence of agonists such as polyunsaturated fatty acids (PUFA). OBJECTIVE: Evaluate the influence of dietary fat in glicidic metabolism in morbidly obese women with Pro12Pro genotype in the gene PPARgamma2. METHODS: Were selected 25 women with genotype Pro12Pro. The fat intake was estimated by food records, being used for the division of groups, GA (until 30% of the total energy expenditure (TEE)) and GB (greater than 30% of the TEE). Biochemical and anthropometric evaluations were conducted in fasting, following the test meal high in n-6 PUFA and postprandial biochemical evaluations. IR and insulin sensitivity (IS) were assessed by HOMA-IR (Homeostasis Model Assessment) and QUICKI (Quantitative Insulin Sensitivity Check Index), respectively. RESULTS AND DISCUSSION: GA presented normal HOMAIR and QUICKI. GB presented higher body mass index (BMI), HOMA-IR, saturated fatty acids (SFA) and monounsaturated (MUFA) intake higher, compared with GA (p < 0.05). In GA, the MUFA intake was negatively correlated with HOMA-IR, fasting glucose and insulin, and positively with QUICKI. The fat and SFA intake contributed to the increase in body mass and IR. However, MUFA intake may have reduced the impact of high fat diet in glicidic metabolism. It is suggested that obese women with Pro12Pro genotype in the PPARgamma2 gene avoid high fat and SFA diets, prioritizing MUFA for controlling obesity and improving the IS.

Influencia de la grasa de la dieta en el metabolismo glucídico de mujeres obesas con el genotipo Pro12Pro en el gen PPARgama2 / Influence of fat diet in glicidic metabolism in obese women with pro12pro genotype in ppargamma2 gene

Introducción: El receptor activado por proliferadores de peroxisomas (PPARγ2) es un factor de transcripción adipogénico que influye en la resistencia a la insulina (RI) en la presencia de agonistas como los ácidos grasos poliinsaturados (AGPI). Objetivo: Evaluar la influencia de la grasa de la dieta en el metabolismo glucídico de mujeres con obesidad mórbida y con el genotipo Pro12Pro en el gen PPARγ2. Métodos: Fueron seleccionadas 25 mujeres con genotipo Pro12Pro. La ingesta habitual de lípidos fue estimada por registros alimentarios, siendo utilizada para la división de los grupos, GA (hasta un 30% del valor energético total (VET)) y GB (por encima de un 30% del VET). Fueron realizadas evaluaciones bioquímicas y antropométricas en ayuno, siguiendo la comida test rica en AGPI n-6 y los análisis bioquímicos postprandiales en GA y GB. La RI y la sensibilidad a la insulina (SI) fueron evaluadas por HOMA-IR (Homeostasis Model Assessment) y QUICKI (Quantitative Insulin Sensitivity Check Index), respectivamente. Resultados y discusión: GA presentó HOMA-IR y QUICKI normales. GB presentó el índice de masa corporal (IMC), HOMA-IR, ingesta de ácidos grasos saturados (AGS) y monoinsaturados (AGMI) superiores a GA (p < 0,05). En GB, los AGMI se correlacionaron negativamente con HOMA-IR, glucosa e insulina en ayuno, y positivamente con QUICKI. Los lípidios totales y AGS contribuyeron al aumento de la masa corporal y RI. Sin embargo, los AGMI parecen reducir el impacto de la dieta hiperlipídica en el metabolismo glucídico. Se propone que mujeres obesas con el genotipo Pro12Pro en el gen PPARγ2 eviten dietas ricas en lípidos y AGS, priorizando AGMI para el control de la obesidad y mejora de la SI (AU)

Introduction: The peroxisome proliferator-activated receptor gamma 2 (PPARγ2) is an adipogenic transcription factor that influences in insulin resistance (IR) in the presence of agonists such as polyunsaturated fatty acids (PUFA). Objective: Evaluate the influence of dietary fat in glicidic metabolism in morbidly obese women with Pro12Pro genotype in the gene PPARγ2. Methods: Were selected 25 women with genotype Pro12Pro. The fat intake was estimated by food records, being used for the division of groups, GA (until 30% of the total energy expenditure (TEE)) and GB (greater than 30% of the TEE). Biochemical and anthropometric evaluations were conducted in fasting, following the test meal high in n-6 PUFA and postprandial biochemical evaluations. IR and insulin sensitivity (IS) were assessed by HOMA-IR (Homeostasis Model Assessment) and QUICKI (Quantitative Insulin Sensitivity Check Index), respectively. Results and discussion: GA presented normal HOMAIR and QUICKI. GB presented higher body mass index (BMI), HOMA-IR, saturated fatty acids (SFA) and monounsaturated (MUFA) intake higher, compared with GA (p < 0.05). In GA, the MUFA intake was negatively correlated with HOMA-IR, fasting glucose and insulin, and positively with QUICKI. The fat and SFA intake contributed to the increase in body mass and IR. However, MUFA intake may have reduced the impact of high fat diet in glicidic metabolism. It is suggested that obese women with Pro12Pro genotype in the PPARγ2 gene avoid high fat and SFA diets, prioritizing MUFA for controlling obesity and improving the IS (AU)