Dietary calcium impairs tomato lycopene bioavailability in healthy humans.

Lycopene (LYC) bioavailability is relatively low and highly variable, because of the influence of several factors. Recent in vitro data have suggested that dietary Ca can impair LYC micellarisation, but there is no evidence whether this can lead to decreased LYC absorption efficiency in humans. Our objective was to assess whether a nutritional dose of Ca impairs dietary LYC bioavailability and to study the mechanism(s) involved. First, in a randomised, two-way cross-over study, ten healthy adults consumed either a test meal that provided 19-mg (all-E)-LYC from tomato paste or the same meal plus 500-mg calcium carbonate as a supplement. Plasma LYC concentration was measured at regular time intervals over 7 h postprandially. In a second approach, an in vitro digestion model was used to assess the effect of increasing Ca doses on LYC micellarisation and on the size and zeta potential of the mixed micelles produced during digestion of a complex food matrix. LYC bioavailability was diminished by 83 % following the addition of Ca in the test meal. In vitro, Ca affected neither LYC micellarisation nor mixed micelle size but it decreased the absolute value of their charge by 39 %. In conclusion, a nutritional dose of Ca can impair dietary LYC bioavailability in healthy humans. This inhibition could be due to the fact that Ca diminishes the electrical charge of micelles. These results call for a thorough assessment of the effects of Ca, or other divalent minerals, on the bioavailability of other carotenoids and lipophilic micronutrients.

Net flux of folates and vitamin B12 through the gastrointestinal tract and the liver of lactating dairy cows.

In study 1, four cows had a ruminal canula, a catheter in the right ruminal vein and an ultrasonic flow probe around the right ruminal artery; a catheter was placed in the auricular artery on experimental days. Blood samples were taken every 10 min from -20 to 60 min after ruminal infusion of 5.79 mmol pteroylmonoglutamic acid and cyanocobalamin. There was a net release of these vitamins across the rumen wall following the infusion (P=0.06). In studies 2 and 3, four cows had catheters in the portal, one hepatic and two mesenteric veins and one mesenteric artery. Plasma flow was determined using p-aminohippurate. In study 2, blood samples were taken before and every 30 min for 6 h after feeding 0 or 4 mg of pteroylmonoglutamic acid. Flow of folates through the portal-drained viscera (PDV) and the total splanchnic tissues (TSP) tended to increase with the ingestion of pteroylmonoglutamic acid (P=0.19). In study 3, blood samples were collected every 30 min for the first 3 h to calculate plasma flow and basal net fluxes of folates and vitamin B12. The cows were fed 2.6 g pteroylmonoglutamic acid and 500 mg cyanocobalamin; blood samples were taken every 2 h for 24 h. Vitamin supplements increased the net release of folates and vitamin B12 from PDV (P=0.04) and TSP (P=0.13). The present results demonstrate that, in dairy cows, at doses reported to improve animal performance, passage of pteroylmonoglutamic acid to the portal blood appears during the 6 h following its ingestion, whereas for cyanocobalamin, it is a slow process, not yet completed 24 h after its ingestion.