Viviane Tyssandier

Main factors governing the transfer of carotenoids from emulsion lipid droplets to micelles.

Carotenoids might lower the incidence of several diseases, yet the mechanisms governing their intestinal absorption are still poorly understood. The aim was to identify and study the main factors governing the transfer of carotenoids from emulsion lipid droplets to mixed micelles, presumed to be a key step in carotenoid absorption. An in vitro model was devised to measure the transfer, and a factorial design was applied to identify the main factors affecting the transfer. Experiments were then conducted to assess the effect of physiological variations of the main factors on the transfer efficiency. Finally, different carotenoids were simultaneously incorporated in emulsion lipid droplets to determine whether they interacted during the transfer. The factorial design gave three factors that significantly affected the transfer: type of carotenoid, pH, and bile lipid concentration. The transfer was (i) inversely related to carotenoid hydrophobicity, (ii) maximum between pH 6 and 7, (iii) maximum from 2 mmol/l bile salts, (iv) impaired by other carotenoids in the case of carotenes, but not in the case of xanthophylls. The transfer mainly depends on carotenoid hydrophobicity, pH, and bile lipid concentration. Physiological variations in pH and bile lipid concentration markedly affect the transfer. Both carotenes and xanthophylls can impair the transfer of carotenes, whereas they have apparently no effect on the transfer of xanthophylls.

Simple method for clinical determination of 13 carotenoids in human plasma using an isocratic high-performance liquid chromatographic method.

We report a reversed-phase high-performance liquid chromatography method which resolves 13 identified carotenoids and nine unknown carotenoids from human plasma. A Nucleosil C18 column and a Vydac C18 column in series are used with an isocratic solvent system of acetonitrile-methanol containing 50 mM acetate ammonium-dichloromethane-water (70:15:10:5, v/v/v/v) as mobile phase at a flow-rate of 2 ml/min. The intra-day (4.5-8.3%) and inter-day (1.3-12.7%) coefficients of variation are suitable for routine clinical determinations.

Carotenoids, Mostly the Xanthophylls, Exchange Between Plasma Lipoproteins

Carotenoids are exclusively transported by lipoproteins; in vitro studies suggest that they might protect these particles against oxidation. Little is known about the factors that govern the distribution of these micronutrients among lipoproteins. The objective of this study was to assess whether carotenoids are exchanged between lipoproteins and what factors, if any, were involved. In the first experiment, different groups of trout were fed for five days with either a carotenoid-free diet or with diets containing 80 mg pure carotenoid per kilogram of feed. Lipoproteins were separated by ultracentrifugation and carotenoid-rich, high-density lipoproteins (HDL) were incubated for two hours at 37 degrees C with carotenoid-free, very low-density lipoproteins (VLDL), and vice versa. After incubation, lipoproteins were re-separated and carotenoids were quantified to measure the transfer. The same experiments were done in the presence of cholesteryl ester transfer protein (CETP) and lecithin cholesterol acyltransferase (LCAT) inhibitors. In a second experiment, the exchange was measured between human VLDL and HDL. In trout, incubation of carotenoid-rich HDL with carotenoid-free VLDL resulted in the appearance of carotenoids in VLDL, and inversely. The higher the hydrophobicity of a carotenoid, the lower its proportion in HDL after incubation. CETP and LCAT inhibitors significantly increased the proportion of carotenoids in HDL after incubation. Results obtained with human lipoproteins showed that the xanthophyll lutein transferred between lipoproteins, but could not show any carotenes (alpha-carotene, beta-carotene, and lycopene) transfer. We conclude that carotenoids, chiefly the xanthophylls, exchange between lipoproteins. The transfer depends on plasma factor(s) sensitive to CETP and/or LCAT inhibitors.

Short-term supplementation with lutein affects biomarkers of lutein status similarly in young and elderly subjects.

There is evidence that lutein may protect against age-related macular degeneration, cataract, cancers and cardiovascular diseases, but no data have been published on the effect of age on lutein status. The purpose of this work was to determine whether there are major differences in the status of this carotenoid between young and elderly subjects. Initial lutein status and the effect of a 5-week lutein supplementation (9 mg/d) on the most common markers of lutein status were compared in 12 young (26.9+/-0.8yr) and 17 older subjects (67.3+/-1.1yr). Lutein was measured by HPLC in fasting serum, adipose tissue and buccal mucosa cells (BMC) before and after supplementation. Macular pigment optical density (MPOD), which partly depends on retina lutein concentration, was measured by reflectometry before and after supplementation. Initial lutein status was not significantly different between the two groups, irrespective of the lutein status marker. Plasma and BMC lutein concentrations significantly increased in both groups after lutein supplementation, but not MPOD or adipose tissue lutein. Plasma and BMC responses to lutein supplementation (percent variation from initial values) were not significantly different between the two groups. These results suggest that there is no major effect of age on lutein status in healthy subjects.

Age-associated B vitamin deficiency as a determinant of chronic diseases

The number of elderly individuals is growing rapidly worldwide and degenerative diseases constitute an increasing problem in terms of both public health and cost. Nutrition plays a role in the ageing process and there has been intensive research during the last decade on B vitamin-related risk factors in vascular and neurological diseases and cancers. Data from epidemiological studies indicate that subclinical deficiency in most water-soluble B vitamins may occur gradually during ageing, possibly due to environmental, metabolic, genetic, nutritional and pathological determinants, as well as to lifestyle, gender and drug consumption. Older adults have distinct absorption, cell transport and metabolism characteristics that may alter B vitamin bioavailability. Case-control and longitudinal studies have shown that, concurrent with an insufficient status of certain B vitamins, hyperhomocysteinaemia and impaired methylation reactions may be some of the mechanisms involved before a degenerative pathology becomes evident. The question that arises is whether B vitamin inadequacies contribute to the development of degenerative diseases or result from ageing and disease. The present paper aims to give an overview of these issues at the epidemiological, clinical and molecular levels and to discuss possible strategies to prevent B vitamin deficiency during ageing.