The production of experimental vitamin A deficiency in rats and mice

Moore, Thomas; Holmes, Paula

doi:10.1258/002367771781006492

Cited by 24 publications

(7 citation statements)

References 7 publications

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“…However, it is likely that this discrepancy is caused by high hepatic retinoid concentrations at the beginning of the study by [18] since (a) WT and BCMO1 -/-breeders were not subjected to a diet depleted of vitamin A, and (b) the duration of the b-carotene/low vitamin A feeding period was shorter than in the study from [29]. Indeed, it has been shown that it is very difficult to trigger vitamin A deficiency in mice after weaning [53]. Thus, considering the current evidence, BCMO1 appears as being the sole enzyme involved in the conversion of b-carotene into retinal.…”

Section: Carotenoid Oxygenasesmentioning

confidence: 98%

β-Carotene conversion products and their effects on adipose tissue

et al. 2009

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Recent epidemiological data suggest that b-carotene may be protective against metabolic diseases in which adipose tissue plays a key role. Adipose tissue constitutes the major b-carotene storage tissue and its functions have been shown to be modulated in response to b-carotene breakdown products, especially retinal produced after cleavage by b-carotene 15,15 0 -monooxygenase (BCMO1), and retinoic acid arising from oxidation of retinal. However, the possibility exists that b-carotene in its intact form can also affect adipocyte function. Development of a knock out model and identification of a loss-offunction mutation have pointed out BCMO1 as being probably the sole enzyme responsible for provitamin A conversion into retinal in mammals. The utilisation of BCMO1 -/-mice should provide insights on b-carotene effect on its own in the future. In humans, intervention studies have highlighted the huge interindividual variation of b-carotene conversion efficiency, possibly due to genetic polymorphisms, which might impact on response to b-carotene. This brief review discusses the processes involved in b-carotene conversion and the effect of cleavage products on body fat and adipose tissue function.

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Section: Carotenoid Oxygenasesmentioning

confidence: 98%

β-Carotene conversion products and their effects on adipose tissue

et al. 2009

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“…However, as a fat-soluble vitamin, it is difficult to establish VAD in the adult rodent as stores are developed early in life. Thus, in the rodent model, it is recommended to begin VAD in utero to ensure adequate signs of deficiency, including growth retardation, by adolescence (Moore and Holmes 1971). A continuation of the VAD diet needs to be followed through lactation, weaning, and adulthood to adequately develop the effects associated with VAD in humans.…”

Section: Animal Models and Research Design Considerationsmentioning

confidence: 99%

The role of micronutrients in the response to ambient air pollutants: Potential mechanisms and suggestions for research design

Miller

Rayalam

2017

Journal of Toxicology and Environmental Health, Part B

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People living in regions of low socioeconomic status are thought to be prone to higher exposures to environmental pollutants, poor nutrition, and numerous preventable diseases and infections. Poverty correlates with pollution and malnutrition; however, limited studies examined their interrelationship. The well-studied, deleterious health effects attributed to environmental pollutants and poor nutrition may act in combination with produce more severe adverse health outcomes than any one factor alone. Deficiencies in specific nutrients render the body more susceptible to injury which may influence the pathways that serve as the mechanistic responses to ambient air pollutants. This review (1) explores specific micronutrients that are of global concern, (2) explains how these nutrients may impact the body's response to ambient air pollution, and (3) provides guidance on designing animal models of nutritional deficiency. It is likely that those individuals who reside in regions of high ambient air pollution are similarly malnourished. Therefore, it is important that research identifies specific nutrients of concern and their impact in identified regions of high ambient air pollution.

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“…Rbp4 is required for transport of hepatic retinol to peripheral tissues, so tissue retinoids in Rbp4 -/-mice are primarily derived from dietary retinyl ester incorporated into chylomicrons. Thus, unlike wild-type mice that have large hepatic retinol stores (Moore and Holmes, 1971) and are difficult to deplete (ClagettDame and DeLuca, 2002;Wolf, 1984), Rbp4 -/-mice can be rapidly depleted of peripheral tissue retinoids by removing vitamin A from the diet. For these studies, Rbp4 -/-mice were deprived of dietary retinol starting at E7.5, 48 hours before crest-derived precursors enter the bowel.…”

Section: Vitamin a Deficiency Causes Hscr-like Distal Bowel Aganglionmentioning

confidence: 99%

Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation

et al. 2010

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SUMMARYHirschsprung disease is a serious disorder of enteric nervous system (ENS) development caused by the failure of ENS precursor migration into the distal bowel. We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinolbinding-protein-deficient (Rbp4 -/-) mice. Ret heterozygosity increases the incidence and severity of distal bowel aganglionosis induced by vitamin A deficiency in Rbp4 -/-animals. Furthermore, RA reduces phosphatase and tensin homolog (Pten) accumulation in migrating cells, whereas Pten overexpression slows ENS precursor migration. Collectively, these data support the hypothesis that vitamin A deficiency is a non-genetic risk factor that increases Hirschsprung disease penetrance and expressivity, suggesting that some cases of Hirschsprung disease might be preventable by optimizing maternal nutrition. MATERIALS AND METHODS Mice Rbp4-/- (Quadro et al., 2005) and Ret +/-mice (Enomoto et al., 2001) were bred >10 generations to C57BL/6. For timed breeding studies, the day of the vaginal plug was considered as embryonic day 0.5 (E0.5). Wild-type CF-1 mice were from Charles River. Mice were maintained on Purina PICO irradiated mouse diet 5058 until E7.5. Food was changed to synthetic chow (El Mel, St Charles, MO, USA) containing sufficient vitamin A (TestDiet 5755; 22.1 IU vitamin A/g) or to vitamin A deficient food (TestDiet 5822; <0.4 IU vitamin A/g) colored blue or yellow to avoid confusion. Mice were maintained on synthetic diets until analysis. Retinoid measurementsRA was quantified using an API-4000 (Applied Biosystems) LC/MS/MS with atmospheric pressure chemical ionization in positive ion mode. Retinol and retinyl esters were quantified by HPLC/UV (Kane et al., 2008a). Tissues were harvested under yellow light, immediately frozen in liquid N 2 and kept at -80°C until assay. Samples were homogenized on ice, extracted and analyzed as described (Kane et al., 2005;Kane et al., 2008b). Total protein was determined by Bradford (Bio-Rad). Slice cultureE12.5 CF-1 midgut sections (300-400 m length) from 400 m proximal to the cecum were cultured on fibronectin-coated (250 g/ml) dishes in Opti-MEM (Invitrogen), glutamine (2 mM), penicillin 100 IU/ml and streptomycin 100 g/ml. Immediately after plating, cells were treated with RA (10 -7 M, Sigma, St Louis, MO, USA) or BMS493 (10 -5 M, generously provided by Dr Chris Zusi at Bristol-Myers Squibb). GDNF (100 ng/ml) was added to cultures three hours later. Cultures were maintained for 16 hours before fixation [4% paraformaldehyde (PFA), 10 minutes, 25°C]. Boyden chamberTranswell supports (8.0 m pore size; 0.33 cm 2 area; Corning 3422; Fisher Scientific) were coated on both sides with 10% Matrigel (Fisher Scientific) in PBS (4°C, 18 hours) and rinsed with PBS. Neural crest medium [Dulbecco's modified Eagle medium (DMEM), 10% chick embryo extract, 1% N2 supplement, 2% B27 supplement, penicil...

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The production of experimental vitamin A deficiency in rats and mice

Cited by 24 publications

References 7 publications

β-Carotene conversion products and their effects on adipose tissue

β-Carotene conversion products and their effects on adipose tissue

The role of micronutrients in the response to ambient air pollutants: Potential mechanisms and suggestions for research design

Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation

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