Effect of retinol on iron bioavailability from Iranian bread in a Caco-2 cell culture model

OBJECTIVE: Iron and vitamin A deficiencies are among the most prevalent nutritional problems. There are no data on iron bioavailability in Iran. In addition, interaction of vitamin A with iron bioavailability is not well documented, so we determined iron bioavailability from the most widely consumed food in Iran, lavash bread, and the effect of vitamin A on this bioavailability. METHODS: In vivo human studies for determining iron bioavailability are cumbersome, time consuming, and costly to perform, so we used an in vitro model in Caco-2 cells. Bread samples were digested with or without vitamin A (10 microg/1.0 g of dried bread). We used an iron solution containing vitamin C as a positive control. Iron absorption was measured using 59FeCl3. Bioavailability was defined as the percentage of radiolabeled iron taken up and transferred by Caco-2 cells after 1.5 h of incubation. Experiments were carried out two to four times. RESULTS: Mean +/- standard deviations for iron bioavailability in bread samples digested without or with additional vitamin A and in controls were 2.53 +/- 1.55%, 6.62 +/- 3.40%, and 20.80 +/- 2.30%, respectively (P < 0.001). Vitamin A caused a 2.62-fold increase in iron absorption from bread samples. CONCLUSIONS: Iranian lavash bread has low iron bioavailability, but this can be increased by vitamin A supplementation. Increasing vitamin A intake can be considered as a method for increasing iron bioavailability, thus combating iron and vitamin A deficiencies simultaneously.     

White matter hyperintensities predict amyloid increase in Alzheimer's disease

Impaired amyloid clearance probably contributes to increased amyloid deposition in sporadic Alzheimer's disease (AD). Diminished perivascular drainage due to cerebral small-vessel disease (CSVD) has been proposed as a cause of reduced amyloid clearance. White matter hyperintensities (WMHs) are considered to reflect CSVD and can be measured using fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI). Amyloid deposition can be determined in vivo using Pittsburgh compound B ([(11)C]PiB) positron emission tomography (PET). We aimed to elucidate the association between WMH and the progression of amyloid deposition in patients with AD. Twenty-two patients with probable AD underwent FLAIR-MRI and [(11)C]PiB-PET examinations at baseline (BL) and after a mean follow-up (FU) interval of 28 months. The relationship between BL-WMH and the progression of cerebral amyloid between BL and FU was examined using a regions-of-interest (ROI) approach. The region-specific variability of this relationship was analyzed using a voxel-based method. The longitudinal analysis revealed a statistically significant association between the amount of BL-WMH and the progression of amyloid load between BL and FU (p = 0.006, adjusted R(2) = 0.375, standardized coefficient β = 0.384). The association was particularly observed in parieto-occipital regions and tended to be closer in regions adjacent to the brain surface. According to our knowledge, this is the first in vivo study in human being supporting the hypothesis that impaired amyloid clearance along perivascular drainage pathways may contribute to β-amyloid deposition in sporadic AD. The extent of WMH might be a relevant factor to be assessed in antiamyloid drug trials.