Iron and zinc are essential micronutrients required for growth and health. Deficiencies of these nutrients are highly prevalent among populations, but can be alleviated by supplementation and food fortification. Cross-sectional studies in humans showed positive association of serum zinc levels with hemoglobin and markers of iron status. Dietary restriction of zinc or intestinal specific conditional knock out of ZIP4 (SLC39A4), an intestinal zinc transporter, in experimental animals demonstrated iron deficiency anemia and tissue iron accumulation. Similarly, increased iron accumulation has been observed in cultured cells exposed to zinc deficient media. These results together suggest a potential role of zinc in modulating intestinal iron absorption and mobilization from tissues. Studies in intestinal cell culture models demonstrate that zinc induces iron uptake and transcellular transport via induction of divalent metal iron transporter-1 (DMT1) and ferroportin (FPN1) expression, respectively. It is interesting to note that intestinal cells are exposed to very high levels of zinc through pancreatic secretions, which is a major route of zinc excretion from the body. Therefore, zinc appears to be modulating the iron metabolism possibly via regulating the DMT1 and FPN1 levels. Herein we critically reviewed the available evidence to hypothesize novel mechanism of Zinc-DMT1/FPN1 axis in regulating intestinal iron absorption and tissue iron accumulation to facilitate future research aimed at understanding the yet elusive mechanisms of iron and zinc interactions.
Dietary fat increases carotenoid bioavailability by facilitating their transfer to the aqueous micellar fraction during digestion. However, the specific effect of both quantity and type of dietary fat required for optimal carotenoid absorption remained unexplored. In the present study, the effect of amount and type of vegetable oils on carotenoid micellarization from carrot, spinach, drumstick leaves and papaya using in vitro digestion/Caco-2 cell model have been assessed. Although, dietary fat (0.5-10% w/w) significantly increased the micellarization of carotenoids from all the test foods, the extent of increase was determined by the food matrix (papaya [ drumstick = spinach [ carrot) and polarity of carotenoids (lutein [ b-carotene = a-carotene [ lycopene). Among the dietary fats tested the carotenoid micellarization was twofold to threefold higher with dietary fat rich in unsaturated fatty acids (olive oil = soybean oil = sunflower oil) compared to saturated fatty acids (peanut oil = palm oil [ coconut oil). Intestinal cell uptake of lutein exceeded that of b-carotene from micellar fraction of spinach leaves digested with various oils. However, cellular uptake of b-carotene is depended on the carotenoid content in micellar fraction rather than the type of fat used. Together these results suggest that food matrix, polarity of carotenoids and type of dietary fat determines the extent of carotenoid micellarization from vegetables and fruits.
The effect of red wine (RW), red grape juice (RGJ), green tea (GT), and representative polyphenols on Caco-2 cell (65)Zn uptake was explored. RW, RGJ, and GT enhanced the uptake of zinc from rice matrix. Fractionation of RW revealed that enhancing activity of zinc uptake was exclusively resided in the polyphenol fraction. Among the polyphenols tested, only tannic acid and quercitin stimulated the uptake of zinc while others did not influence the uptake. In tune with these results, only tannic acid and quercitin competed with zinquin (a zinc selective fluorophore) for zinc in vitro. Although all the polyphenols tested appear to enhance the expression of metallothionein (MT), the induction was higher with tannic acid, quercitin, and RW extract. Furthermore, phytic acid abrogated the tannic acid-induced MT expression. These results suggest that polyphenol-rich beverages, tannic acid, and quercitin bind and stimulate the zinc uptake and MT expression in Caco-2 cells.
Objective: To assess the magnitude and determinants of vitamin A deficiency (VAD) and coverage of vitamin A supplementation (VAS) among pre-school children. Design: A community-based cross-sectional study was carried out by adopting a multistage, stratified, random sampling procedure. Setting: Rural areas of eight states in India. Subjects: Pre-school children and their mothers were covered. Results: A total of 71 591 pre-school children were clinically examined for ocular signs of VAD. Serum retinol concentrations in dried blood spots were assessed in a sub-sample of 3954 children using HPLC. The prevalence of Bitot spots was 0?8 %. The total ocular signs were significantly higher (P , 0?001) among boys (2?6 %) compared with girls (1?9 %) and in older children (3-4 years) compared (P , 0?001) with younger (1-2 years), and were also high in children of labourers, scheduled castes and illiterate mothers. The odds of having Bitot spots was highest in children of scheduled caste (OR 5 3?8; 95 % CI 2?9, 5?0), labourers (OR 5 2?9; 95 % CI 2?1, 3?9), illiterate mothers (OR 5 2?7; 95 % CI 2?2, 2?3) and households without a sanitary latrine (OR 5 5?9; 95 % CI 4?0, 8?7). Subclinical VAD (serum retinol level ,20 mg/dl) was observed in 62 % of children. This was also relatively high among scheduled caste and scheduled tribe children. The rate of coverage of VAS was 58 %. Conclusions: The study revealed that VAD is a major nutritional problem and coverage of VAS was poor. The important determinants of VAD were illiteracy, low socio-economic status, occupation and poor sanitation. Strengthening the existing VAS programme and focused attention on dietary diversification are essential for prevention of VAD.
Retinitis Pigmentosa (RP) is a common form of retinal degeneration characterized by photoreceptor degeneration and retinal pigment epithelium (RPE) atrophy causing loss of visual field and acuities. Exome sequencing identified a novel homozygous splice site variant (c.111+1G>A) in the gene encoding retinol binding protein 4 (RBP4). This change segregated with early onset, progressive, and severe autosomal recessive retinitis pigmentosa (arRP) in an eight member consanguineous pedigree of European ancestry. Additionally, one patient exhibited developmental abnormalities including patent ductus arteriosus and chorioretinal and iris colobomas. The second patient developed acne from young age and extending into the 5th decade. Both patients had undetectable levels of RBP4 in the serum suggesting that this mutation led to either mRNA or protein instability resulting in a null phenotype. In addition, the patients exhibited severe vitamin A deficiency, and diminished serum retinol levels. Circulating transthyretin levels were normal. This study identifies the RBP4 splice site change as the cause of RP in this pedigree. The presence of developmental abnormalities and severe acne in patients with retinal degeneration may indicate the involvement of genes that regulate vitamin A absorption, transport and metabolism.
Under gastric conditions, the iron core of pea ferritin is released into the digestive medium due to acid induced structural alterations and dissociation of protein. The released iron interacts with dietary factors leading to modulation of pea ferritin iron bioavailability, resembling the typical characteristics of non-heme iron.
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