Vitamin A deficiency interferes with proliferation and maturation of cells in the chicken small intestine

2000 ◽  
Vol 41 (4) ◽  
pp. 410-415 ◽  
Author(s):  
Z. Uni ◽  
G. Zaiger ◽  
O. Gal-Garber ◽  
M. Pines ◽  
I. Rozenboim ◽  
...  
Keyword(s):  
Small Intestine ◽  
Vitamin A ◽  
Vitamin A Deficiency

scholarly journals Vitamin A deficiency induces morphometric changes and decreased functionality in chicken small intestine

1998 ◽  
Vol 80 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Zehava Uni ◽  
Gidi Zaiger ◽  
Ram Reifen
Keyword(s):  
Enzyme Activity ◽  
Small Intestine ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Control Diet ◽  
Normal Activity ◽  
Cellular Hypertrophy ◽  
Mucosal Morphology ◽  
Mucosal Protein ◽  
Rats And Mice

The effect of vitamin A on chicken intestinal mucosal morphology and functionality was tested in relation to severe and mild vitamin A deficiency and vitamin A repletion. Compared with rats and mice, chickens have a very quick response to a deficient dietary intake. Severe vitamin A deficiency altered the small intestine of chickens at both the biochemical and the morphological levels. It caused the loss of mucosal protein, reduced villus height and crypt depth and diminished activities of disaccharidases, transpeptidase and alkaline phosphate (EC 3.1.3.1). The ratios RNA-.DNA, RNA:protein and protein:DNA, and the DNA concentrations in 1 g intestinal tissue, together with morphological measurements, provided knowledge about the pattern of lesion. The results indicated that (1) lack of vitamin A influenced cellular hyperplasia as it caused an increase in DNA content and in the number of enterocytes per villus; (2) lack of vitamin A influenced cellular hypertrophy as it decreased the protein:DNA ratio. There was no difference in mucosal enzyme activity between the two deficient groups. The repletion group exhibited a remarkable increase in mucosal enzyme activity only 4 d after switching to the control diet. The evidence presented in our paper suggests that the low vitamin A supply interferes with the normal activity of chicken intestinal mucosa as it influences the processes of proliferation and maturation of enterocytes.

scholarly journals The interaction of vitamin A deficiency and rotavirus infection in the mouse

1990 ◽  
Vol 63 (2) ◽  
pp. 363-373 ◽  
Author(s):  
Faruk Ahmed ◽  
David B. Jones ◽  
Alan A. Jackson
Keyword(s):  
Small Intestine ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Control Diet ◽  
Relative Weight ◽  
Liver Weight ◽  
Mucosal Barrier ◽  
Spleen Weight ◽  
Deficient Diet ◽  
Rotavirus Infection

Weanling mice were fed on a control dietad lib., a vitamin A-deficient dietad lib.or pair-fed to the intake of the vitamin A-deficient group. Vitamin A deficiency was induced by 63–70 d of age. On day 77 mice were given 30 μl rotavirus/mouse orally and examined histologically 1 week later. There were no changes in relative liver weight in any of the groups, but following infection animals deficient in vitamin A showed a significant increase in spleen weight compared with the other groups. The relative weight of the thymus was reduced by vitamin A deficiency, in both non-infected and infected animals. The histology of the spleen, thymus and small intestine was similar in all three dietary groups before infection. The number of goblet cells per duodenal villus in vitamin A-deficient animals was significantly lower than that of control and pair-fed animals. In the small intestine of vitamin A-deficient animals, rotavirus infection caused dramatic changes to the mucosa, with almost complete destruction of the tips of the villi, but control and pair-fed animals had normal villi. It is concluded that although rotavirus infection and vitamin A-deficiency cause few changes alone, in their action together there is significant destruction of the mucosal barrier of the small intestine.

scholarly journals Cell Type-specific Expression of β-Carotene 9', 10'-Monooxygenase in Human Tissues

2005 ◽  
Vol 53 (11) ◽  
pp. 1403-1412 ◽  
Author(s):  
Annika Lindqvist ◽  
Yu-Guang He ◽  
Stefan Andersson
Keyword(s):  
Small Intestine ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Physiological Role ◽  
Cell Types ◽  
Human Tissues ◽  
Specific Expression ◽  
Β Carotene

The symmetrically cleaving β-carotene 15, 15'-monooxygenase (BCO1) catalyzes the first step in the conversion of provitamin A carotenoids to vitamin A in the mucosa of the small intestine. This enzyme is also expressed in epithelia in a variety of extraintestinal tissues. The newly discovered β-carotene 9', 10'-monooxygenase (BCO2) catalyzes asymmetric cleavage of carotenoids. To gain some insight into the physiological role of BCO2, we determined the expression pattern of BCO2 mRNA and protein in human tissues. By immunohistochemical analysis it was revealed that BCO2 was detected in cell types that are known to express BCO1, such as epithelial cells in the mucosa of small intestine and stomach, parenchymal cells in liver, Leydig and Sertoli cells in testis, kidney tubules, adrenal gland, exocrine pancreas, and retinal pigment epithelium and ciliary body pigment epithelia in the eye. BCO2 was uniquely detected in cardiac and skeletal muscle cells, prostate and endometrial connective tissue, and endocrine pancreas. The finding that the BCO2 enzyme was expressed in some tissues and cell types that are not sensitive to vitamin A deficiency and where no BCO1 has been detected suggests that BCO2 may also be involved in biological processes other than vitamin A synthesis.

scholarly journals RNAseq studies reveal distinct transcriptional response to vitamin A deficiency in small intestine versus colon, uncovering novel vitamin A-regulated genes

2019 ◽  
Author(s):  
Zhi Chai ◽  
Yafei Lyu ◽  
Qiuyan Chen ◽  
Cheng-Hsin Wei ◽  
Lindsay M. Snyder ◽  
...  
Keyword(s):  
Small Intestine ◽  
Vitamin A ◽  
Target Genes ◽  
Vitamin A Deficiency ◽  
Expression Patterns ◽  
Differentially Expressed Gene ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Increased Risk ◽  
The Impact

AbstractVitamin A (VA) deficiency remains prevalent in resource limited countries, affecting over 250 million preschool aged children. Vitamin A deficiency is associated with reduced intestinal barrier function and increased risk of mortality due to mucosal infection. Using Citrobacter rodentium (C. rodentium) infection in mice as a model for diarrheal diseases in humans, previous reports showed reduced pathogen clearance and survival in vitamin A deficient (VAD) mice compared to their vitamin A sufficient (VAS) counterparts.ObjectivesTo characterize and compare the impact of preexisting VA deficiency on gene expression patterns in the small intestine (SI) and the colon, and to discover novel target genes in VA-related biological pathways.MethodsVAD mice were generated by feeding VAD diet to pregnant C57/BL6 dams and their post-weaning offspring. RNAseq were performed using the total mRNAs extracted from SI and colon. Differentially Expressed Gene (DEG), Gene Ontology (GO) enrichment, and Weighted Gene Co-expression Network Analysis (WGCNA) were performed to characterize expression and co-expression patterns.ResultsDEGs compared between VAS and VAD groups detected 49 SI and 94 colon genes. By GO information, SI DEGs were significantly enriched in categories relevant to retinoid metabolic process, molecule binding, and immune function. Immunity related pathways, including “humoral immune response” and “complement activation” were positively associated with VA in SI. Three co-expression modules showed significant correlation with VA status in SI; these modules contained four known retinoic acid targets. In addition, other SI genes of interest (e.g. Mbl2, Cxcl14, and Nr0b2) in these modules were suggested as new candidate genes regulated by VA. Furthermore, our analysis showed that markers of two cell types in SI, mast cells and Tuft cells, were significantly altered by VA status. In colon, “cell division” was the only enriched category and was negatively associated with VA. Thus, comparison of co-expression modules between SI and colon indicated distinct networks under the regulation of dietary VA and suggest that preexisting VAD could have a significant impact on the host response to a variety of disease conditions.

Quantification of Vitamin A in Fortified Rapeseed, Groundnut and Soya Oils Using a Simple Portable Device: Comparison to High Performance Liquid Chromatography

2013 ◽  
Vol 83 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Cécile Renaud ◽  
Jacques Berger ◽  
Arnaud Laillou ◽  
Sylvie Avallone
Keyword(s):  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Vitamin A ◽  
High Performance ◽  
Vitamin A Deficiency ◽  
Developed Countries ◽  
Portable Device ◽  
Least Developed Countries ◽  
Control Food ◽  
Assay Precision

Vitamin A deficiency is still one of the major public health problems in least developed countries. Fortification of vegetable oils is a strategy implemented worldwide to prevent this deficiency. For a fortification program to be effective, regular monitoring is necessary to control food quality in the producing units. The reference methods for vitamin A quantification are expensive and time-consuming. A rapid method should be useful for regular assessment of vitamin A in the oil industry. A portable device was compared to high-performance liquid chromatography (HPLC) for three plant oils (rapeseed, groundnut, and soya). The device presented a good linearity from 3 to 30 mg retinol equivalents per kg (mg RE.kg- 1). Its limits of detection and quantification were 3 mg RE.kg- 1 for groundnut and rapeseed oils and 4 mg RE.kg- 1 for soya oil. The intra-assay precision ranged from 1.48 % to 3.98 %, considered satisfactory. Accuracy estimated by the root mean squares error ranged from 3.99 to 5.49 and revealed a lower precision than HPLC (0.4 to 2.25). Although it offers less precision than HPLC, the device estimates quickly the vitamin A content of the tested oils from 3 or 4 to 15 mg RE.kg- 1.

Research Recommendations for Applying Vitamin A-Labelled Isotope Dilution Techniques to Improve Human Vitamin A Nutrition

2014 ◽  
Vol 84 (Supplement 1) ◽  
pp. 52-59 ◽  
Author(s):  
Sherry A. Tanumihardjo ◽  
Anura V. Kurpad ◽  
Janet R. Hunt
Keyword(s):  
Public Health ◽  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Human Subjects ◽  
The Body ◽  
Pool Size ◽  
Serum Retinol ◽  
Vitamin A Status ◽  
Status Assessment ◽  
Total Body

The current use of serum retinol concentrations as a measurement of subclinical vitamin A deficiency is unsatisfactory for many reasons. The best technique available for vitamin A status assessment in humans is the measurement of total body pool size. Pool size is measured by the administration of retinol labelled with stable isotopes of carbon or hydrogen that are safe for human subjects, with subsequent measurement of the dilution of the labelled retinol within the body pool. However, the isotope techniques are time-consuming, technically challenging, and relatively expensive. There is also a need to assess different types of tracers and doses, and to establish clear guidelines for the use and interpretation of this method in different populations. Field-friendly improvements are desirable to encourage the application of this technique in developing countries where the need is greatest for monitoring the risk of vitamin A deficiency, the effectiveness of public health interventions, and the potential of hypervitaminosis due to combined supplement and fortification programs. These techniques should be applied to validate other less technical methods of assessing vitamin A deficiency. Another area of public health relevance for this technique is to understand the bioconversion of β-carotene to vitamin A, and its relation to existing vitamin A status, for future dietary diversification programs.

Vitamin A deficiency is associated with disease severity in patients with liver cirrhosis

2020 ◽  
Author(s):  
M Nagel ◽  
C Labenz ◽  
M Nguyen-Tat ◽  
N Cabezas Wallscheid ◽  
C Czauderna ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Vitamin A ◽  
Disease Severity ◽  
Vitamin A Deficiency

Mitral Valve Replacement in an Adult with Left Pulmonary Agenesis

2015 ◽  
Vol 18 (3) ◽  
pp. 109
Author(s):  
Huseyin Saskin ◽  
Mustafa Idiz ◽  
Cagri Duzyol ◽  
Huseyin Macika ◽  
Rezan Aksoy
Keyword(s):  
Mitral Valve ◽  
Vitamin A ◽  
Valve Replacement ◽  
Viral Infections ◽  
Vitamin A Deficiency ◽  
Pulmonary Agenesis ◽  
Pulmonary Vessels ◽  
Live Births ◽  
Factors Associated ◽  
Female Predominance

Pulmonary agenesis is associated with the absence of pulmonary vessels, bronchi, or parenchyma. This condition usually occurs between the 4th and 5th week of gestation during the embryonic phase. Etiopathogenic factors associated with pulmonary agenesis are not fully understood. In the literature, genetic and teratogenic factors, viral infections, and vitamin-A deficiency are shown to be associated with pulmonary agenesis [Malcon 2012]. This condition may be seen unilaterally or bilaterally. Although the precise rate of incidence is unknown, it is estimated to occur in one of every 10,000 to 12,000 live births [Yetim 2011]. There is a 1.3:1 female predominance with unilateral agenesis [Halilbasic 2013]

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