Recientemente se ha descrito que los portadores del alelo minoritario 2 (1/2) en el exón 1 del gen del receptor scavenger clase B tipo I (SR-BI) son más susceptibles a la presencia de grasa saturada en la dieta, con un mayor aumento del colesterol ligado a lipoproteínas de baja densidad (cLDL). Nuestro objetivo es determinar si dicho polimorfismo puede influir también en el metabolismo lipoproteico posprandial, ya que se ha señalado que puede mediar en la absorción intestinal de los triglicéridos.
Diseño y métodosSe seleccionó a 47 voluntarios normolipémicos, homocigotos para el alelo e3 de la apolipoproteína (apo) E —37 homocigotos para el alelo 1 del SR-BI (1/1) y 10 heterocigotos para el alelo 2 (1/2)—. Recibieron una comida grasa (1 g/kg de peso corporal, 60.000 unidades de vitamina A por m2 de superficie corporal y 7 mg de colesterol/kg de peso), con un 60% de calories como grasa, un 15% como proteínas y un 25% como hidratos de carbono. Se realizaron extracciones en el tiempo 0 y cada hora hasta las 6 h y otras dos últimas a las 8,5 y 11 h, determinándose el colesterol, los triglicéridos, la apo A-I y la apo B.
ResultadosSe observó una interacción entre el polimorfismo presente en el exón 1 del gen del SRBI y los valores de triglicéridos totales en function del tiempo (p = 0,029). Así, los portadores del alelo 2 (1/2) presentaron una curva más retrasada, lo que indica una absorción intestinal más lenta de triglicéridos que los homocigotos 1/1.
ConclusionesNuestros datos indican que los portadores del alelo minoritario 2, con genotipo 1/2, presentan una absorción intestinal retrasada de triglicéridos. Esto podría explicar parte de la diferencia interindividual en la respuesta lipémica posprandial.
Carriers of the minority allele 2 (1/2) in exon 1 of the scavenger receptor class B type I (SR-BI) gene have recently been reported to be more susceptible to the presence of saturated fat in diet, with a greater increase in low-density lipoprotein cholesterol. The aim of this study was to determine whether this polymorphism can also influence postprandial lipoprotein metabolism, since it has been described as a possible mediator in intestinal triglyceride absorption.
Design and methodsForty-seven normolipidemic volunteers who were homozygotes for the e3 allele of apolipoprotein (apo) e were selected [37 homozygotes for allele 1 of the SR-BI (1/1) gene and 10 heterozygotes for allele 2 (1/2)]. The volunteers were given a fatty meal containing 1 g fat/kg of body weight, 60,000 IU of vitamin A per m2 of body surface and 7 mg of cholesterol/kg of body weight), with 60% of calories as fat, 15% as proteins and 25% as carbohydrates. Blood samples were taken at time 0, every hour until hour 6 and every 2 h and 30 min until hour 11 to determine concentrations of cholesterol, triglycerides, apo A-1 and apo B.Forty-seven normolipidemic volunteers who were homozygotes for the e3 allele of apolipoprotein (apo) e were selected [37 homozygotes for allele 1 of the SR-BI (1/1) gene and 10 heterozygotes for allele 2 (1/2)]. The volunteers were given a fatty meal containing 1 g fat/kg of body weight, 60,000 IU of vitamin A per m2 of body surface and 7 mg of cholesterol/kg of body weight), with 60% of calories as fat, 15% as proteins and 25% as carbohydrates. Blood samples were taken at time 0, every hour until hour 6 and every 2 h and 30 min until hour 11 to determine concentrations of cholesterol, triglycerides, apo A-1 and apo B.
ResultsInteraction between the presence of polymorphism exon 1 variant at the SR-BI gene locus and total triglyceride levels was observed according to time (p = 0.029). Thus, carriers of allele 2 (1/2) presented a later curve, suggesting slower intestinal triglyceride absorption than homozygotes 1/1.
ConclusionsOur data suggest that carriers of the minority allele 2 with genotype 1/2 present slower intestinal triglyceride absorption, which could explain the individual variability observed in postprandial lipemic response.