Changes in lipoprotein subfractions following menopause in the Longitudinal Study of Adult Health (ELSA-Brasil).

INTRODUCTION: It is unclear how aging and menopause-induced lipid changes contribute to the elevated cardiovascular risk in menopausal women. We examined the association between lipid profiles and menopausal status and duration of menopause in the Longitudinal Study of Adult Health (ELSA-Brasil). METHODS: This is a cross-sectional analysis of baseline data from women in the ELSA-Brasil, stratified by duration of menopause into 5 groups: pre-menopause, <2 years, 2-5.9 years, 6-9.9 years and ≥10 years of menopause, excluding menopause <40 years or of non-natural cause; also excluded were women using lipid-lowering drugs or hormone replacement. Comparisons were performed using ANOVA with Bonferroni correction. Associations of menopause categories and time since menopause with lipid variables obtained by vertical auto-profile were tested using multiple linear regression. RESULTS: From 1916 women, postmenopausal groups had unadjusted higher total cholesterol, LDL-c, real LDL-c, IDL-c, VLDL-c, triglycerides, non-HDL-c, VLDL3-c, triglyceride-rich lipoprotein remnants (TRL-c) and buoyant LDL-c concentrations than pre-menopausal women, with no difference among postmenopausal groups. In multiple linear regression, duration of menopause <2 years was significantly associated with TRL-c [7.21 mg/dL (95% CI 3.59-10.84)] and VLDL3-c [2.43 mg/dL (95%CI 1.02-3.83)]. No associations of menopausal categories with HDL-c or LDL-c subfractions were found, and nor were associations of time since menopause with lipid subfractions. CONCLUSIONS: In a large sample of Brazilian women, deterioration of the lipid profile following menopause was confirmed, which could contribute to the increased cardiovascular risk. Our findings suggest a postmenopausal elevation in triglyceride-rich lipoprotein remnants. How lipoprotein subfractions change after the onset of menopause warrants investigation in studies with appropriate designs.

Los triglicéridos y la aterogénesis / Triglycerides and atherogenesis

ResumenLas lipoproteínas ricas en triglicéridos (TRL) comprenden los quilomicrones, las VLDL y sus remanentes. Las TRL son altamente heterogéneas, difiriendo en el tamaño, densidad, composición y riesgo cardiovascular asociado. La evidencia acumulada demuestra una fuerte correlación entre el riesgo de enfermedad cardiovascular (ECV) y el nivel de TAG en ayunas y no en ayunas (posprandial). Se han propuesto dos mecanismos por los cuales las TRL pueden incrementar la ateroesclerosis: los remanentes de TRL y las VLDL son capaces de penetrar la íntima arterial, pueden ser internalizados por los macrófagos y convertirlos en células espumosas. Segundo: durante la lipólisis de las TRL se liberan un número de lípidos inflamatorios que alteran la biología del endotelio. Los TAG no son directamente aterogénicos, pero representan un importante biomarcador de ECV a causa de su asociación con una alta concentración de partículas pequeñas y densas de LDL, niveles reducidos de colesterol HDL y con apo C-III, una proteína proinflamatoria y proaterogénica.

AbstractTriglyceride-rich lipoproteins (TRL) comprise chylomicrons, VLDL and their remnants. TRL are highly heterogeneous, differing in size, density, composition, and associated cardiovascular risk. Accumulating evidence demonstrates a strong correlation between the risk of cardiovascular disease (CVD) and both non-fasting (postprandial) and fasting plasma TAG level. Two mechanisms by which TRL might increase atherosclerosis are proposed: TRL remnants and VLDL are able to penetrate the arterial intima, can be internalized by macrophages and convert these cells into foam cells. Second: during lipolysis of TRL a number of inflammatory lipids are released that alter endothelial biology. TAG are not directly atherogenic but represent an important biomarker of CVD because of their association with a high concentration of small dense LDL particles, reduced HDL cholesterol levels, and with apo C-III, a proinflammatory and proatherogenic protein.