Effect of Vitamin C Deficiency in Guinea Pigs on Intestinal Functions and Chemical Composition of Brush Border Membrane

1981 ◽  
Vol 25 (4) ◽  
pp. 213-220 ◽  
Author(s):  
R.M. Dulloo ◽  
S. Majumdar ◽  
R.N. Chakravarti ◽  
S.K. Mehta ◽  
A. Mahmood
2016 ◽  
Vol 36 (7) ◽  
pp. 696-702 ◽  
Author(s):  
Stine N. Hansen ◽  
Janne G. Schjoldager ◽  
Maya D. Paidi ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg

1991 ◽  
Vol 260 (1) ◽  
pp. G108-G118 ◽  
Author(s):  
W. H. Karasov ◽  
B. W. Darken ◽  
M. C. Bottum

We measured ascorbic acid (AA) uptake across the intestinal brush border in vitro in intact tissue from guinea pigs fed maintenance AA (200 mg/kg diet) or made hypervitaminotic (5,000 mg/kg diet) or hypovitaminotic (chronically and acutely). Total uptake per centimeter ileum was 25-50% lower in hypervitaminotic juvenile, adult male, and lactating guinea pigs compared with their respective controls, whereas carrier-mediated D-glucose uptake and Na(+)-independent AA uptake were similar. High dietary ascorbate specifically reduced the Vmax for carrier-mediated AA uptake. Hypovitaminosis had no significant effect on uptake of AA or other solutes. We performed diet-switching experiments (high-AA diet to maintenance diet) with young and adult guinea pigs to determine the reversibility of the downregulation. In adult guinea pigs, the downregulation of AA uptake was reversible within 7 days. In the young of mothers fed high AA during pregnancy and lactation, and which fed on high AA for 14 days after weaning, the downregulation was reversible within 14 days. Thus regulation of AA uptake is reversible and therefore probably does not play a significant role in the development of vitamin C dependency in human adults, or their young, after ingestion of megadoses of ascorbic acid.


2014 ◽  
Vol 34 (7) ◽  
pp. 639-645 ◽  
Author(s):  
Ditte Søgaard ◽  
Maiken M. Lindblad ◽  
Maya D. Paidi ◽  
Stine Hasselholt ◽  
Jens Lykkesfeldt ◽  
...  

2010 ◽  
Vol 105 (1) ◽  
pp. 54-61 ◽  
Author(s):  
Henriette Frikke-Schmidt ◽  
Pernille Tveden-Nyborg ◽  
Malene Muusfeldt Birck ◽  
Jens Lykkesfeldt

Vitamin C deficiency – or hypovitaminosis C defined as a plasma concentration below 23 μm – is estimated to affect hundreds of millions of people in the Western world, in particular subpopulations of low socio-economic status that tend to eat diets of poor nutritional value. Recent studies by us have shown that vitamin C deficiency may result in impaired brain development. Thus, the aim of the present study was to investigate if a poor diet high in fat and cholesterol affects the vitamin C status of guinea pigs kept on either sufficient or deficient levels of dietary ascorbate (Asc) for up to 6 months with particular emphasis on the brain. The present results show that a high-fat and cholesterol diet significantly decreased the vitamin C concentrations in the brain, irrespective of the vitamin C status of the animal (P < 0·001). The brain Asc oxidation ratio only depended on vitamin C status (P < 0·0001) and not on the dietary lipid content. In plasma, the levels of Asc significantly decreased when vitamin C in the diet was low or when the fat/cholesterol content was high (P < 0·0001 for both). The Asc oxidation ratio increased both with low vitamin C and with high fat and cholesterol content (P < 0·0001 for both). We show here for the first time that vitamin C homoeostasis of brain is affected by a diet rich in fat and cholesterol. The present findings suggest that this type of diet increases the turnover of Asc; hence, individuals consuming high-lipid diets may be at increased risk of vitamin C deficiency.


1967 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
W. E. J. Phillips

The effect of administration of ascorbic acid to normal or vitamin A-deficient rats was studied in relation to hepatic levels of ubiquinones and sterols. Similar studies were made on tissues from guinea pigs deficient in vitamin C, vitamin A, or both. Vitamin A deficiency increased the concentration of liver ubiquinones in the rat. Administration of ascorbate did not influence tissue levels of ubiquinones or sterols. Vitamin C deficiency increased the concentration of sterols but not of ubiquinones in the liver of the guinea pig. Vitamin A deficiency did not increase ubiquinones nor did a combined deficiency of vitamins A and C. A secondary effect of vitamin C deficiency in the vitamin A-deficient rat is not the cause of increased ubiquinone levels.


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