scholarly journals High dietary fat and cholesterol exacerbates chronic vitamin C deficiency in guinea pigs

2010 ◽  
Vol 105 (1) ◽  
pp. 54-61 ◽  
Author(s):  
Henriette Frikke-Schmidt ◽  
Pernille Tveden-Nyborg ◽  
Malene Muusfeldt Birck ◽  
Jens Lykkesfeldt
Keyword(s):  
Vitamin C ◽  
Guinea Pigs ◽  
Cholesterol Content ◽  
Dietary Lipid ◽  
Western World ◽  
High Fat ◽  
Vitamin C Deficiency ◽  
Increased Risk ◽  
Oxidation Ratio ◽  
The Brain

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.

scholarly journals Vitamin C deficiency in weanling guinea pigs: differential expression of oxidative stress and DNA repair in liver and brain

2007 ◽  
Vol 98 (6) ◽  
pp. 1116-1119 ◽  
Author(s):  
Jens Lykkesfeldt ◽  
Gilberto Perez Trueba ◽  
Henrik E. Poulsen ◽  
Stephan Christen
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Vitamin C ◽  
Lipid Oxidation ◽  
Protein Oxidation ◽  
Guinea Pigs ◽  
Vitamin C Deficiency ◽  
Markers Of Oxidative Stress ◽  
Selective Preservation ◽  
The Brain

Neonates are particularly susceptible to malnutrition due to their limited reserves of micronutrients and their rapid growth. In the present study, we examined the effect of vitamin C deficiency on markers of oxidative stress in plasma, liver and brain of weanling guinea pigs. Vitamin C deficiency caused rapid and significant depletion of ascorbate (P < 0·001), tocopherols (P < 0·001) and glutathione (P < 0·001), and a decrease in superoxide dismutase activity (P = 0·005) in the liver, while protein oxidation was significantly increased (P = 0·011). No changes in lipid oxidation or oxidatively damaged DNA were observed in this tissue. In the brain, the pattern was markedly different. Of the measured antioxidants, only ascorbate was significantly depleted (P < 0·001), but in contrast to the liver, ascorbate oxidation (P = 0·034), lipid oxidation (P < 0·001), DNA oxidation (P = 0·13) and DNA incision repair (P = 0·014) were all increased, while protein oxidation decreased (P = 0·003). The results show that the selective preservation of brain ascorbate and induction of DNA repair in vitamin C-deficient weanling guinea pigs is not sufficient to prevent oxidative damage. Vitamin C deficiency may therefore be particularly adverse during the neonatal period.

scholarly journals Vitamin C Deficiency in the Young Brain—Findings from Experimental Animal Models †

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1685
Author(s):  
Pernille Tveden-Nyborg
Keyword(s):  
Animal Models ◽  
Vitamin C ◽  
Experimental Animal ◽  
Western World ◽  
Comprehensive Overview ◽  
Experimental Animal Models ◽  
Vitamin C Deficiency ◽  
The Brain

Severe and long-term vitamin C deficiency can lead to fatal scurvy, which is fortunately considered rare today. However, a moderate state of vitamin C (vitC) deficiency (hypovitaminosis C)—defined as a plasma concentration below 23 μM—is estimated to affect up to 10% of the population in the Western world, albeit clinical hallmarks in addition to scurvy have not been linked to vitC deficiency. The brain maintains a high vitC content and uniquely high levels during deficiency, supporting vitC’s importance in the brain. Actions include both antioxidant and co-factor functions, rendering vitamin C deficiency likely to affect several targets in the brain, and it could be particularly significant during development where a high cellular metabolism and an immature antioxidant system might increase sensitivity. However, investigations of a non-scorbutic state of vitC deficiency and effects on the developing young brain are scarce. This narrative review provides a comprehensive overview of the complex mechanisms that regulate vitC homeostasis in vivo and in the brain in particular. Functions of vitC in the brain and the potential consequences of deficiency during brain development are highlighted, based primarily on findings from experimental animal models. Perspectives for future investigations of vitC are outlined.

Maternal vitamin C deficiency does not reduce hippocampal volume and β-tubulin III intensity in prenatal Guinea pigs

2016 ◽  
Vol 36 (7) ◽  
pp. 696-702 ◽  
Author(s):  
Stine N. Hansen ◽  
Janne G. Schjoldager ◽  
Maya D. Paidi ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Vitamin C ◽  
Guinea Pigs ◽  
Hippocampal Volume ◽  
Maternal Vitamin ◽  
Vitamin C Deficiency ◽  
Β Tubulin

scholarly journals Distribution of vitamin C is tissue specific with early saturation of the brain and adrenal glands following differential oral dose regimens in guinea pigs

2015 ◽  
Vol 113 (10) ◽  
pp. 1539-1549 ◽  
Author(s):  
Stine Hasselholt ◽  
Pernille Tveden-Nyborg ◽  
Jens Lykkesfeldt
Keyword(s):  
Vitamin C ◽  
Guinea Pigs ◽  
Adrenal Glands ◽  
Biological Fluids ◽  
Brain Regions ◽  
Hill Equation ◽  
Distribution Kinetics ◽  
The World ◽  
Dose Concentration ◽  
The Brain

Vitamin C (VitC) deficiency is surprisingly common in humans even in developed parts of the world. The micronutrient has several established functions in the brain; however, the consequences of its deficiency are not well characterised. To elucidate the effects of VitC deficiency on the brain, increased knowledge about the distribution of VitC to the brain and within different brain regions after varying dietary concentrations is needed. In the present study, guinea pigs (like humans lacking the ability to synthesise VitC) were randomly divided into six groups (n 10) that received different concentrations of VitC ranging from 100 to 1500 mg/kg feed for 8 weeks, after which VitC concentrations in biological fluids and tissues were measured using HPLC. The distribution of VitC was found to be dynamic and dependent on dietary availability. Brain saturation was region specific, occurred at low dietary doses, and the dose–concentration relationship could be approximated with a three-parameter Hill equation. The correlation between plasma and brain concentrations of VitC was moderate compared with other organs, and during non-scorbutic VitC deficiency, the brain was able to maintain concentrations from about one-quarter to half of sufficient levels depending on the region, whereas concentrations in other tissues decreased to one-sixth or less. The adrenal glands have similar characteristics to the brain. The observed distribution kinetics with a low dietary dose needed for saturation and exceptional retention ability suggest that the brain and adrenal glands are high priority tissues with regard to the distribution of VitC.

In vivo vitamin C deficiency in guinea pigs increases ascorbate transporters in liver but not kidney and brain

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

INTERRELATIONSHIP OF VITAMINS A AND C ON TISSUE UBIQUINONES AND STEROLS OF RATS AND GUINEA PIGS

1967 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
W. E. J. Phillips
Keyword(s):  
Ascorbic Acid ◽  
Vitamin A ◽  
Vitamin C ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Vitamin A Deficiency ◽  
Secondary Effect ◽  
Vitamin C Deficiency ◽  
Vitamins A And C ◽  
Combined Deficiency

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.

Age and Dietary Vitamin C Intake Affect Brain Physiology in Genetically Modified Mice Expressing Human Lipoprotein(A) and Unable to Synthesize Vitamin C

2021 ◽  
Vol 14 ◽  
Author(s):  
Lei Shi ◽  
Aleksandra Niedzwiecki ◽  
Matthias Rath
Keyword(s):  
Vitamin C ◽  
Oxidative Damage ◽  
Critical Role ◽  
Cholesterol Homeostasis ◽  
Dietary Vitamin ◽  
Brain Health ◽  
Lipoprotein A ◽  
Vitamin C Deficiency ◽  
The Brain

Aims: Lipoprotein (a) deposition in coronary vascular plaques and cerebral vessels is a recognized risk factor for cardiovascular disease, and research supports its role as a “repair factor” in vascular walls weakened by vitamin C deficiency. Background: Humans depend on dietary vitamin C as an important antioxidant, and as a cofactor in collagen synthesis, yet are prone to vitamin C deficiency. The brain is the one with the highest vitamin C content, due to its high oxygen consumption and oxidative stress. It has been shown that brain aging is accompanied by accumulated oxidative damage, which can lead to memory decline and neurological diseases. Objective: Our transgenic mouse, Gulo (-/-); Lp(a)+, presents a unique model for the study of key aspects of human metabolism with respect to a lack of internal vitamin C synthesis and the production of human Lipoprotein(a). Method: This mouse model was used in our study to investigate the effects of prolonged intake of low and high levels of vitamin C, at different ages, on oxidative damage, cholesterol levels and Lipoprotein(a) deposition in the brain. Result: The results show that a long-term high vitamin C intake is important in maintaining brain cholesterol homeostasis and preventing oxidative damage in Gulo(-/-);Lp(a)+ mice as they age. Moreover, we observed that the formation of brain Lipoprotein(a) deposits was negatively correlated with brain level of vitamin C, thereby confirming its role as a stability factor for an impaired extracellular matrix. Conclusion: Our study emphasizes the critical role of vitamin C in protecting brain health as we age. Other: Our findings show that optimal vitamin C intake from early life to old age is important in brain health to prevent oxidative stress damage and to maintain cholesterol homeostasis in the brain. More importantly, negative correlation between brain ascorbic levels and the formation of Lp(a) deposit on the choroid plexus further emphasizes the critical role of vitamin C in protecting brain health throughout the normal aging process.

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