Sex-dependent variables in the modulation of postalimentary lipemia.

OBJECTIVE: To quantify in young adults the sex-dependent differences in lipemic responses to a fat meal, we measured the association of these responses with markers of atherosclerosis and determined their metabolic regulators. METHODS: Forty-nine normolipidemic volunteers, 25 women and 24 men, were matched according to age, body mass index, waist circumference, diet, physical activity, and apolipoprotein-E phenotyping. After receiving a standardized fat meal (40 g of fat/m2 of body surface area), serial blood samples were drawn for laboratory analysis. Common carotid intima-media thickness was measured. RESULTS: The lipemic responses were much greater in men than in women for plasma triacylglycerol (TAG), cholesterol, and TAG in TAG-rich lipoproteins, non-esterified fatty acids, phospholipids, and apolipoprotein-B100. Men presented with increased blood pressure, carotid intima-media thickness, TAG, hepatic lipase, and insulin and lower high-density lipoprotein cholesterol, apolipoprotein-AI, and non-esterified fatty acid concentrations. Only in men did carotid intima-media thickness correlate marginally with titers of autoantibodies to epitopes of oxidized low-density lipoprotein; in addition, phospholipids and cholesteryl esters were negatively related to autoantibodies. Multivariate analysis indicated that age (R2 = 45%), waist circumference (R2 = 19%), phospholipids (R2 = 39%), non-esterified fatty acids (R2 = 29%), insulin (R2 = 17%), lipoprotein lipase activity (R2 = 16%), and cholesteryl ester transfer protein (an exploratory variable; R2 = 6%) are strong determinants of postalimentary lipemia in women and that only insulin (R2 = 55%) and phospholipids (R2 = 37%) are determinants in men. CONCLUSIONS: We have provided data explaining that postalimentary lipemia is differently regulated by sex. Several risk factors for coronary heart disease and significant associations with atherosclerosis biomarkers were found only in men.

Estudo "in vitro" da influência da dessializaçäo de lipoproteínas no transporte reverso de colesterol / Study \"in vitro\" of influence of the lipoprotein desialylation on the reverse cholesterol transport

A dessializaçäo de LDL tem sido descrita como uma lipoproteína aterogênica por promover um acúmulo de lípides em cultura de células. A influência de lipoproteínas dessializadas com neuraminidase no transporte reverso de colesterol foi investigada in vitro utilizando VLDL, LDL,HDL total, 'HDL IND. 2' e 'HDL IND. 3' isoladas do plasma de doadores saudáveis, e macrófagos do peritônio de camundongos. Segundo os resultados obtidos, a dessializaçäo de lipoproteínas significativamente ocasionou: 1) uma diminuiçäo na capacidade de HDL total e 'HDL IND. 2', mas näo a 'HDL .IND 3', de remover o colesterol das clulas; 2)uma reduçäo na taxa de esterificaçäo do colesterol pela LCAT sem modificar a atividade intrínseca da LCAT da HDL; 3) um aumento na transferência de colesterol esterificado mediada pela CETP, de HDL para as lipoproteínas contendo apoB; 4) um aumento na captaçäo de colesterol de HDL e LDL pelos macrófagos, porém a quantidade de colesterol captada de LDL dessializada pelas células foi muito maior que de HDL dessializada. Estas evidências in vitro indicam que, além da dessializaçäo de lipoproteínas aumentar a captaçäo celular de colesterol, pode contribuir para o desenvolvimento prematuro de aterosclerose ao afetar as principais etapas do transporte reverso de colesterol