RESUMEN
Adiponectin is an adipokine inversely correlated with obesity, which has beneficial effect on insulin resistance and lipid metabolism. Considering its potential as a therapeutic target in the metabolic disorder contexts, and in order to add knowledge in the area, our study evaluated the ADIPOQ 276G > T polymorphism effect on adiponectin levels, and on lipoproteins of clinical interest in a population sample composed of 211 healthy individuals. Significant effects were observed only among men: the carriers of heterozygous genotype (GT) showed high levels of adiponectin (p = 0.018), while the rare homozygous genotype (TT) gave its carriers a negative phenotype, represented by higher levels of low density lipoprotein cholesterol (LDL-C) (p = 0.004 and p = 0.005) and total cholesterol (TC) (p = 0.010 and p = 0.005) compared to carriers of other genotypes (GG and GT respectively), the independent effect of SNP on LDL-C and TC levels was confirmed by multiple regression analysis (p = 0.008 and p = 0.044). We found no evidence of correlation between circulating adiponectin levels and biochemical markers, which suggests, therefore, an SNP 276G > T independent effect on adiponectin levels and on lipoprotein metabolism in men enrolled in this study.
RESUMEN
La lipoproteínas remanentes (RLPs) son el producto de la lipólisis de los triglicéridos transportados por las lipoproteínas de baja densidad (VLDL) de origen hepático e intestinal y de los quilomicrones intestinales. Dicha lipólisis es catalizada por la lipoproteína lipasa y se produce en pasos sucesivos, de manera que los productos son heterogéneos. Su concentración plasmática en ayunas es pequeña en pacientes normolipémicos y aumenta en el estado post-prandial. Las alteraciones genéticas en subtipos de su componente Apo-E aumentan notablemente su concentración plasmática y producen el fenotipo de disbetalipoproteinemia. Se las considera aterogénicas porque injurian el endotelio, sufren estrés oxidativo, son captadas por los macrófagos en el subendotelio vascular y generan las células espumosas que son precursoras de ateromas. Su origen metabólico, como productos de varios tipos de lipoproteínas, explican su estructura heterogénea, sus concentraciones plasmáticas variables y las dificultades metodológicas que dificultan su inclusión en el perfil lipoproteico como parte de los estudios epidemiológicos. Los últimos avances en los estudios metabólicos y la actualización de su papel clínico, justifican una revisión de los conocimientos actuales.
Remnant lipoproteins (RLPs) are the lipolytic product of triglycerides transported by very low density lipoproteins (VLDL) of hepatic and intestinal origin and intestinal chylomicrons. Lipoprotein lipase activity hydrolyse triglycerides in several steps, producing heterogeneous particles. Fasting plasma concentration in normolipidemic subjects is low, but it increases in post-prandial states. Genetic alterations in Apo-E subtypes increases RLPs plasma concentration and produce dyslipoproteinemia phenotype. RLPs atherogenicity depends on their role as endothelial injuring factors, their impaired recognition by lipoprotein receptors, and their susceptibility to oxidative stress. They also promote the circulation of molecular adhesion molecules, the internalization in subendothelial macrophages via scavenger receptors and the accumulation in foam cells, all of them early mechanisms of atheromatosis. RLPs metabolism has been a subject of controversial studies. Their origin from different lipoproteins may explain their structural heterogeneity, therefore increasing the methodological difficulties to include RLPs in the atherogenic lipoprotein profile in the epidemiological studies of the field. Last advances on metabolism of RLPs and their emergent clinical role justifies an up dated revision of RLPs.