Enrichment of tomato paste with 6% tomato peel increases lycopene and beta-carotene bioavailability in men.

A high intake of tomato products is associated with a lower incidence of upper aerodigestive tract and prostate cancers. This beneficial effect might be explained by a higher intake of carotenoids such as lycopene and/or beta-carotene. Because tomato peels, usually eliminated during tomato processing, are a valuable source of these carotenoids, we designed a study to examine whether a tomato paste enriched in tomato peels (ETP, 6% peel) increases the absorption of these carotenoids compared to a classically made tomato paste (CTP). Carotenoid bioaccessibility was evaluated using an in vitro digestion model by measuring the amount of carotenoids transferred from the pastes to micelles. Carotenoid absorption by human intestinal cells (Caco-2) was evaluated after the addition of carotenoid-rich micelles (obtained from the in vitro digestion of the 2 pastes). Carotenoid bioavailability in humans was assessed by measuring chylomicron carotenoid responses in a postprandial experiment in which 8 healthy men consumed 2 meals containing either the ETP or the CTP. ETP contained 47.6 mg lycopene (58% more than CTP) and 1.75 mg beta-carotene (99% more than CTP) per 100 g of paste. In micelles, 30% more lycopene and 81% more beta-carotene were recovered after ETP than after CTP in vitro digestion. The amount of carotenoids absorbed by Caco-2 cells was 75% greater (P < or = 0.05) for lycopene and 41% greater (P < or = 0.05) for beta-carotene after the addition of micelles from ETP than from CTP. After ETP intake the chylomicron beta-carotene response was 74% greater than after CTP intake, and the lycopene response tended to be greater (34.1%, P = 0.093). Peel enrichment of tomato paste with tomato peel is an interesting option for increasing lycopene and beta-carotene intakes.

Glycemic and insulinemic meal responses modulate postprandial hepatic and intestinal lipoprotein accumulation in obese, insulin-resistant subjects.

BACKGROUND: Exacerbated postprandial lipemia is a risk factor for cardiovascular disease and is linked to insulin status. Limited data on the effect of dietary carbohydrate on postprandial lipoprotein accumulation are available. OBJECTIVE: We tested the hypothesis that dietary carbohydrates with different glucose availability alter postprandial lipoprotein metabolism differently in obese, insulin-resistant subjects. DESIGN: After an overnight fast, 9 subjects with central obesity and insulin resistance but normal triacylglycerolemia randomly ingested 2 test meals with comparable amounts of fat (28-29 g) and digestible carbohydrate (91-94 g) but with different quantities of slowly available glucose (SAG) in cereal products (17 or 2 g SAG/100 g for biscuits and wheat flakes, respectively). Blood samples were collected before and for 6 h after meal intakes. RESULTS: The postmeal 0-2-h areas under the curve (AUCs) for glycemia and insulinemia were significantly lower (P < 0.05) after the biscuit meal than after the flakes meal. Plasma triacylglycerol concentrations increased significantly after the flakes meal but not after the biscuit meal (1.5-fold higher 0-6-h AUC for the flakes meal). Apolipoprotein B-100 concentrations in the triacylglycerol-rich lipoprotein fraction increased significantly 2 h after the flakes meal but not after the biscuit meal (3-fold higher 0-6-h AUC for the flakes meal). Apolipoprotein B-48 concentrations increased (P < 0.05) 4 h after the flakes meal but not after the biscuit meal (2.3-fold higher 0-6-h AUC for the flakes meal). CONCLUSION: Mixed meals containing slowly digestible carbohydrate that induces low glycemic and insulinemic responses reduce the postprandial accumulation of both hepatically and intestinally derived triacylglycerol-rich lipoproteins in obese subjects with insulin resistance.

Glucose and galactose regulate intestinal absorption of cholesterol.

A dose-dependent increase in cholesterol absorption was induced by glucose addition (0-75 mM) to the apical medium of TC7 cells, a well-characterized clone of Caco-2. The uptake into the cells and the secretion rate to the basolateral space were both enhanced by glucose and galactose. This up-regulation was suppressed by SGLT1 inhibition but not by GLUT2 inhibition. Cholesterol cell uptake was significantly decreased by PMA and increased by chelerythrine, with more pronounced changes in the presence of hexoses. Thus, the involvement of a protein kinase C signalling pathway was evidenced in the regulation processes of intestinal cholesterol absorption. In the presence of antibodies directed to hSR-BI cholesterol absorption was reduced by 40% and glucose or galactose no longer enhanced it. We suggest that glucose or galactose, through an interaction with SGLT1, activates a protein kinase C pathway that regulates the activity of one of the intestinal cholesterol transporters, namely hSR-BI.

Amounts and types of fatty acids in meals affect the pattern of retinoids secreted in human chylomicrons after a high-dose preformed vitamin A intake.

High doses of preformed vitamin A are commonly used to correct vitamin A deficiency. Newly absorbed vitamin A is secreted mainly as retinyl esters in chylomicrons. The effect of changing types and amounts of fatty acids on fatty acid composition of chylomicron retinoid esters when a high dose of vitamin A is ingested have not been studied previously. In the present study, 10 healthy young men ingested, in a random order, mixed meals containing 15,000 retinol equivalents (RE) of vitamin A (as retinyl palmitate) and either no fat or 40 g of fat provided as butter, olive oil, or sunflower oil. Fasting and postprandial blood samples were obtained for 7 hours after meals. Free retinol and the main retinyl esters (retinyl palmitate/oleate, stearate, and linoleate) were measured in chylomicrons by high-performance liquid chromatography (HPLC). Chylomicron retinyl palmitate/oleate and retinyl stearate concentrations significantly increased after intake of the 4 test meals. Conversely, chylomicron retinyl linoleate and chylomicron free retinol significantly increased only after the sunflower and the fat-free meals, respectively. The main retinoid secreted in chylomicrons after the intake of the fat-rich meals was retinyl palmitate/oleate, accounting for 63% to 79% of total RE, but it was free retinol after the fat-free meal (51% of total RE). Thus, the retinoid pattern secreted in chylomicrons after the intake of a high dose of preformed vitamin A depends on type and amounts of fatty acids ingested. To explain this result we suggest that the esterification process of retinol in the enterocyte by lecithin:retinol acyltransferase can be overwhelmed by a high load of vitamin A. Consequently, a significant proportion of the retinol is esterified by acyl coenzyme A:retinol acyltransferase (ARAT) with ingested fatty acids, explaining the appearance of retinyl linoleate in chylomicrons after the sunflower oil meal. If a high dose of preformed vitamin A is ingested with a fat-free meal, a significant proportion of retinol is not esterified, owing to the lack of fatty acids for ARAT, which explains the appearance of free retinol in chylomicrons.

Butter differs from olive oil and sunflower oil in its effects on postprandial lipemia and triacylglycerol-rich lipoproteins after single mixed meals in healthy young men.

Accumulation of postprandial triacylglycerol-rich lipoproteins is generated by assimilation of ingested dietary fat and has been increasingly related to atherogenic risk. Nevertheless, the influence of different kinds of dietary fatty acids on postprandial lipid metabolism is not well established, except for (n-3) polyunsaturated long-chain fatty acids. Our goal was to evaluate the effects of test meals containing a common edible fat source of saturated (butter), monounsaturated (olive oil) or (n-6) polyunsaturated (sunflower oil) fatty acids on postprandial lipid and triacylglycerol-rich lipoprotein responses. After a 12-h fast, 10 healthy young men ingested mixed meals containing 0 g (control) or 40 g fat, provided as butter, olive oil or sunflower oil in a random order. Fasting and postmeal blood samples were collected for 7 h. The no-fat test meal did not elicit any change over baseline except for plasma phospholipids, insulin and nonesterified fatty acids. Conversely, the three fat-containing meals elicited bell-shaped postprandial changes (P < 0.05) in serum triacylglycerols, free and esterified cholesterol, and nonesterified fatty acids. The butter meal induced a lower postprandial rise of triacylglycerols in serum and chylomicrons (incremental AUC, mmol.h/L: 0.72) than the two unsaturated oils (olive oil: 1.6, sunflower oil: 1.8), which did not differ. Circulating chylomicrons were smaller after the butter meal than after the two vegetable oil meals. The in vitro susceptibility of circulating chylomicrons to hydrolysis by postheparin plasma was higher after sunflower oil than after butter or olive oil. We conclude that butter results in lower postprandial lipemia and chylomicron accumulation in the circulation of young men than olive or sunflower oils after consumption of a single mixed meal.

Functional characterization of three clones of the human intestinal Caco-2 cell line for dietary lipid processing.

We aimed to improve the use of the human intestinal Caco-2 cell line for studying dietary lipid and cholesterol processing by using isolated pure clones (Chantret et al. 1994). Three clones (TC7, PD7 and PF11) were grown as monolayers on semi-permeable filters and compared for cell viability, fatty acid and cholesterol apical uptake or basolateral secretion, apolipoprotein B-48 basolateral secretion and 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activity. The TC7 clone showed the best viability upon apical incubation with mixed micelles and should be preferred for routine work. Short-term (3.0 h) rates of apical uptake of cholesterol were not different with the three clones, whereas the rate of apical uptake of oleic acid (18:1) was lower (P<0.05) with PF11 (250.6 nmol/mg) and the basolateral secretion of cholesterol and oleic acid was lower with the TC7 clone (0.40 and 29.1 nmol/mg respectively). The secretion of apolipoprotein B-48 basolaterally was about 2-fold lower than from PD7 clone. The basal levels of HMG-CoA reductase activity were significantly different (P<0.05; TC7>PF11 >PD7). The down-regulation of the enzyme activity was moderate (range 13.8-21.0%) and comparable in the presence of apical micellar cholesterol, but was much marked upon basolateral incubation with LDL (range 34.0-53.6%), especially for the PD7 clone. In conclusion, the Caco-2 clones characterized here proved to be particularly suitable for studying lipid nutrients processing. Because these three clones exhibit some different metabolic capabilities, they provide a new tool to study intestinal response to lipid nutrients.

Biliary anionic peptide fraction and apoA-I regulate intestinal cholesterol uptake.

Evidence is now in favor of protein-facilitated mechanisms for the intestinal cholesterol absorption. Here we report that the unesterified cholesterol uptake by rat jejunal brush border membrane vesicles (BBMVs) is efficient, saturable, and protein-mediated. The human apolipoproteins biliary anionic peptide factor (APF) and A-I (apoA-I) up-regulate micellar cholesterol uptake in a dose-dependent manner, but for all tested concentrations (0.1-20 microM), the lipid-free APF was more efficient than apoA-I. This uptake stimulation was suppressed after addition of Pabs directed to the external lipid-binding domain of the CLA-1/SR-BI and reduced by Pabs directed to the external loop of CD36. Thus, CLA-1/SR-BI and to a lesser extent CD36 are involved in the regulation of intestinal cholesterol uptake. APF, the main protein bound to biliary lipids, is likely one of their physiological effectors. As APF is an unesterified cholesterol carrier, it could facilitate the intestinal absorption of biliary cholesterol.