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 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 Effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus infection in mice

1991 ◽  
Vol 65 (3) ◽  
pp. 475-485 ◽  
Author(s):  
Faruk Ahmed ◽  
David B. Jones ◽  
Alan A. Jackson
Keyword(s):  
Immune Response ◽  
Vitamin A ◽  
Antibody Production ◽  
Vitamin A Deficiency ◽  
Control Diet ◽  
Serum Antibody ◽  
Cell Mediated Immunity ◽  
Deficient Diet ◽  
Antibody Levels ◽  
Deficient Group

The effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus was studied in mice. The virus was given by oral dosing or by intraperitoneal injection. For oral challenge, weanling mice were fed on either a control or vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. A fourth group was fed on the vitamin Adeficient diet ad lib. for 10 weeks and then refed the control diet for 2 weeks. On day 77, mice were each given 30 μl EDIM rotavirus orally and the animals were killed and examined 1 week later. The delayedtype hypersensitivity (DTH) response to picryl chloride was measured as an index of cell-mediated immunity. For intraperitoneal challenge, weanling mice were fed on either the control diet or the vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. On day 77, mice were each injected intraperitoneally with 30 μl EDIM rotavirus and 1 week later antibody production was measured. In both experiments the body-weight, liver and serum vitamin A levels of the vitamin A-deficient group were significantly lower than the control or pair-fed groups. Following oral dosing the serum antibody levels specific to rotavirus were statistically significantly lower in vitamin Adeficient animals than the control or pair-fed groups. Vitamin A-deficient mice also showed an impaired DTH response compared with the control and pair-fed animals. Animals refed vitamin A for a short period showed a partial restoration of the antibody response. Following intraperitoneal challenge no statistically significant changes were observed in the serum antibody levels between any of the dietary groups. It is concluded that vitamin A deficiency impaired antibody production when rotavirus was given orally. Vitamin A deficiency also impaired cell-mediated immunity.

Vitamin A Status and Hepatic Drug Metabolism in the Rat

1973 ◽  
Vol 51 (1) ◽  
pp. 6-11 ◽  
Author(s):  
G. C. Becking
Keyword(s):  
Vitamin A ◽  
Drug Metabolism ◽  
Vitamin A Deficiency ◽  
Hepatic Drug Metabolism ◽  
Deficient Diet ◽  
Hepatic Drug ◽  
Vitamin A Status ◽  
Cytochrome P 450 ◽  
Liver Vitamin

The effect of vitamin A status on hepatic drug metabolism was studied in rats. Animals were fed diets with and without vitamin A for 20 and 25 days. Weight gains of control and deficient animals were not significantly different, whereas liver vitamin A levels had decreased to less than 10% of control animals after 20 days and were essentially zero after eating the deficient diet for 25 days. Aniline metabolism in vitro and aminopyrine metabolism in vitro and in vivo were significantly lower in male weanling rats fed a vitamin A deficient diet for 20 days. No alteration in in vitro p-nitrobenzoic acid metabolism was noted after 25 days on the test. Vitamin A deficiency did not alter microsomal protein levels or cytochrome c reductase activity but deficient animals did have a lower microsomal cytochrome P-450 content. Hepatic enzyme activities and cytochrome P-450 levels were restored to values approaching those found in control animals by feeding vitamin A deficient rats the vitamin A containing diet for 21 days. Liver vitamin A levels were markedly increased after re-feeding studies but were still significantly lower than control animals.

scholarly journals Effects of food or nutrient restriction on milk vitamin A transfer and neonatal vitamin A stores in the rat

1990 ◽  
Vol 63 (2) ◽  
pp. 351-362 ◽  
Author(s):  
Ana Maria ◽  
G. Pasatiempo ◽  
A. Catharine Ross
Keyword(s):  
Vitamin A ◽  
Maternal Diet ◽  
Control Diet ◽  
Serum Vitamin ◽  
Liver Weight ◽  
Retinol Binding Protein ◽  
Serum Retinol ◽  
Total Food Intake ◽  
Affect Transfer ◽  
Liver Vitamin

We have investigated the effects of maternal diets low in fat or protein, or restricted in total food intake on vitamin A transfer from the dam to her pups. When animals were fed on diets moderately restricted in fat or protein, minimal differences in milk, serum, and liver vitamin A concentrations were observed compared with animals fed on a control diet. In a second study, dams were fed on diets more severely restricted in protein, or fat, or both, or were fed on a control diet equal to 50% of the intake of control rats but containing an equal amount of vitamin A. The quantity of milk obtained from these more severely restricted dams' nipples or the pups' stomachs was greatly reduced; however, there were no differences in milk vitamin A concentration. Body-weight, liver weight, and total liver vitamin A stores of undernourished pups were just half those measured for control pups, although serum vitamin A and serum retinol-binding protein were nearly normal in concentration. We conclude that (a) moderate restrictions in fat or protein in the maternal diet are insufficient to affect transfer of vitamin A to the suckling pup; (b) further dietary restrictions could cause decreased milk production with little change in milk vitamin A concentration and, hence, (c) the neonates' hepatic retinol accumulation during the suckling period is markedly reduced when maternal diets are severely deficient in fat or protein or of normal composition but restricted in amount.

scholarly journals The effect of vitamin A deficiency on hepatic, renal and pulmonary glutathione S-transferase activities in the rat

1980 ◽  
Vol 188 (3) ◽  
pp. 889-893 ◽  
Author(s):  
Z H Siddik ◽  
E G Mimnaugh ◽  
M A Trush ◽  
T E Gram
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Nutritional State ◽  
Glutathione S Transferase ◽  
Chemical Carcinogens ◽  
Deficient Diet ◽  
Liver Cytosol ◽  
Weanling Rats ◽  
Glutathione S Transferases ◽  
The Relationship

Feeding male weanling rats on a vitamin A-deficient diet for 6 weeks resulted in significant increases (44-57%) in glutathione S-aryl-, S-aralkyl- S-alkyl- and S-epoxidetransferase activities in the liver cytosol. Only the S-aralkyl- (27%) and S-alkyltransferase (14%) activities were significantly increased in the kidney as a result of deficiency. There was no effect on any of the pulmonary glutathione S-transferase activities. The increases in hepatic transferase activities were due primarily to increases (25-96%) in the apparent Vmax. There were no changes in the apparant Km of any of the four drug substrates employed. With 3,4-dichloronitrobenzene as the second substrate, the apparent Km for glutathione was increased by over 2-fold in vitamin A-deficient livers as compared with controls. The relationship between these results and enhanced susceptibility to chemical carcinogens in vitamin A deficiency is briefly discussed, and comparison is made between the effects of this nutritional state and pretreatment with drug inducers on the glutathione S-transferases.

Effect of intestinal resection and arginine-free diet on rat physiology

1995 ◽  
Vol 269 (2) ◽  
pp. G313-G318 ◽  
Author(s):  
Y. Wakabayashi ◽  
E. Yamada ◽  
T. Yoshida ◽  
N. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Small Intestine ◽  
Nitrogen Balance ◽  
Control Diet ◽  
Intestinal Resection ◽  
Dependent Manner ◽  
Deficient Diet

The small intestine has been presumed to release citrulline as a precursor for the endogenous arginine synthesis. We studied the effect of intestinal resection and arginine-free diet on rat physiology. We maintained rats with massively resected small intestine (R rats) and those with transected intestines (T rats) on either control or an arginine-free diet. After 4 wk, R rats fed deficient diet [R(-)] lost weight by a mean of 46 g, whereas R rats fed control diet [R(+)] and T rats fed control [T(+)] and deficient diet [T(-)] gained 30-96 g. Average nitrogen balance was 150, 60, 110, and -33 mg/day for T(+), T(-), R(+), and R(-), respectively. The concentrations of arginine in skeletal muscle were 654, 163, 230, and 84 nmol/g, respectively, and those in plasma were 133, 50, 103, and 54 microM, respectively. The concentrations of citrulline in R rats were halved compared with T rats irrespective of diet. We conclude that arginine is synthesized in a small intestine-dependent manner in the rat.

scholarly journals Vitamin A-Deficient Diet Accelerated Atherogenesis in Apolipoprotein E−/−Mice and Dietaryβ-Carotene Prevents This Consequence

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Noa Zolberg Relevy ◽  
Dror Harats ◽  
Ayelet Harari ◽  
Ami Ben-Amotz ◽  
Rafael Bitzur ◽  
...  
Keyword(s):  
Vitamin A ◽  
Apolipoprotein E ◽  
Vitamin A Deficiency ◽  
Plasma Cholesterol ◽  
Atherosclerotic Lesion ◽  
Dietary Vitamin ◽  
Control Group ◽  
Chow Diet ◽  
Deficient Diet ◽  
Aortic Sinus

Vitamin A is involved in regulation of glucose concentrations, lipid metabolism, and inflammation, which are major risk factors for atherogenesis. However, the effect of vitamin A deficiency on atherogenesis has not been investigated. Therefore, the objective of the current study was to examine whether vitamin A deficiency accelerates atherogenesis in apolipoprotein E-deficient mice (apoE−/−). ApoE−/−mice were allocated into the following groups: control, fed vitamin A-containing chow diet; BC, fed chow diet fortified withDunaliellapowder containingβc isomers; VAD, fed vitamin A-deficient diet; and VAD-BC group, fed vitamin A-deficient diet fortified with aDunaliellapowder. Following 15 weeks of treatment, liver retinol concentration had decreased significantly in the VAD group to about 30% that of control group. Vitamin A-deficient diet significantly increased both plasma cholesterol concentrations and the atherosclerotic lesion area at the aortic sinus (+61%) compared to the control group. Dietaryβc fortification inhibited the elevation in plasma cholesterol and retarded atherogenesis in mice fed the vitamin A-deficient diet. The results imply that dietary vitamin A deficiency should be examined as a risk factor for atherosclerosis and that dietaryβc, as a sole source of retinoids, can compensate for vitamin A deficiency.

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 Methionine plus Cystine Levels for Light Laying Hens on Growth Phase

2021 ◽  
Vol 1 (53) ◽  
pp. 180
Author(s):  
Marcelo Helder Medeiros Santana ◽  
Fernando Guilherme Perazzo Costa ◽  
Ricardo Romão Guerra ◽  
Jalceyr Pessoa Figueiredo Júnior ◽  
Matheus Ramalho De Lima ◽  
...  
Keyword(s):  
Serum Protein ◽  
Laying Hens ◽  
Control Diet ◽  
Relative Weight ◽  
Spleen Weight ◽  
Feed Conversion ◽  
Final Body Weight ◽  
Linear Effect ◽  
Protein Levels ◽  
Different Levels

<p>The aim of this study was to evaluate the methionine plus cystine levels in the diets of laying hens during the rearing period (13-18 weeks old). The diets included a control diet formulated according to NRC and five other diets with different levels of this digestible methionine plus cystine (0.317, 0.356, 0.396, 0.436 and 0.475%) that have been based on the recommendations of the Brazilian poultry and swine tables. Performance, serological and histological variables were evaluated. There was linear effect on final body weight, weight gain, methionine plus cystine intake and feed conversion, and quadratic effect on the serum albumin levels, serum protein levels and relative spleen weight. The estimated level of digestible methionine plus cystine were 0.361%, 0.346% and 0.398%, for albumin activity, serum protein and relative weight of spleen, respectively. The different formulation bases significantly influenced the histology of the liver, small intestine and magnum. It is recommended the use of levels above 0.475% of digestible methionine plus cystine for light laying hens with 13-18 weeks old, which corresponded to a ratio of digestible methionine plus cystine: digestible lysine of more than 98%.</p>

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