Nutrición Hospitalaria (Aug 2010)
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
Abstract
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 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.
