scholarly journals Vitamin C Deficiency May Delay Diet-Induced NASH Regression in the Guinea Pig

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 69
Author(s):  
Josephine Skat-Rørdam ◽  
Kamilla Pedersen ◽  
Gry Freja Skovsted ◽  
Ida Gregersen ◽  
Sara Vangsgaard ◽  
...  
Keyword(s):  
Vitamin C ◽  
Guinea Pig ◽  
Diet Change ◽  
Low Fat ◽  
Alcoholic Fatty Liver ◽  
Vitamin C Deficiency ◽  
Beneficial Role ◽  
Low Fat Diet ◽  
Hepatic Transcriptome

Oxidative stress is directly linked to non-alcoholic fatty liver disease (NAFLD) and the progression to steaotohepatitis (NASH). Thus, a beneficial role of antioxidants in delaying disease progression and/or accelerating recovery may be expected, as corroborated by recommendations of, e.g., vitamin E supplementation to patients. This study investigated the effect of vitamin C deficiency—often resulting from poor diets low in fruits and vegetables and high in fat—combined with/without a change to a low fat diet on NAFLD/NASH phenotype and hepatic transcriptome in the guinea pig NASH model. Vitamin C deficiency per se did not accelerate disease induction. However, the results showed an effect of the diet change on the resolution of hepatic histopathological hallmarks (steatosis, inflammation, and ballooning) (p < 0.05 or less) and indicated a positive effect of a high vitamin C intake when combined with a low fat diet. Our data show that a diet change is important in NASH regression and suggest that a poor vitamin C status delays the reversion towards a healthy hepatic transcriptome and phenotype. In conclusion, the findings support a beneficial role of adequate vitamin C intake in the regression of NASH and may indicate that vitamin C supplementation in addition to lifestyle modifications could accelerate recovery in NASH patients with poor vitamin C status.

scholarly journals Atorvastatin and Vitamin E Accelerates NASH Resolution by Dietary Intervention in a Preclinical Guinea Pig Model

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2834 ◽  
Author(s):  
Julie Hviid Klaebel ◽  
Mia Skjødt ◽  
Josephine Skat-Rørdam ◽  
Günaj Rakipovski ◽  
David H. Ipsen ◽  
...  
Keyword(s):  
Vitamin E ◽  
Guinea Pig ◽  
Target Genes ◽  
Dietary Intervention ◽  
Liver Weight ◽  
Diet Change ◽  
Lifestyle Modifications ◽  
Low Fat ◽  
Low Fat Diet ◽  
Guinea Pig Model

Despite affecting millions of patients worldwide, no pharmacological treatment has yet proved effective against non-alcoholic steatohepatitis (NASH) induced liver fibrosis. Current guidelines recommend lifestyle modifications including reductions in dietary energy intake. Recently, therapy with atorvastatin and vitamin E (vitE) has been recommended, although clinical studies on the resolution of hepatic fibrosis are inconclusive. Targeting NASH-induced hepatic end-points, this study evaluated the effects of atorvastatin and vitE alone or in combination with a dietary intervention in the guinea pig NASH model. Guinea pigs (n = 72) received 20 weeks of high fat feeding before allocating to four groups: continued HF feeding (HF), HF diet with atorvastatin and vitE (HF+), low-fat diet (LF) and low-fat with atorvastatin and vitE (LF+), for four or eight weeks of intervention. Both LF and LF+ decreased liver weight, cholesterol and plasma dyslipidemia. LF+ further improved hepatic histopathological hallmarks (p < 0.05), liver injury markers aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (p < 0.05) and reduced the expression of target genes of hepatic inflammation and fibrosis (p < 0.05), underlining an increased effect on NASH resolution in this group. Collectively, the data support an overall beneficial effect of diet change, and indicate that atorvastatin and vitE therapy combined with a diet change act synergistically in improving NASH-induced endpoints.

scholarly journals Early Life Vitamin C Deficiency Does Not Alter Morphology of Hippocampal CA1 Pyramidal Neurons or Markers of Synaptic Plasticity in a Guinea Pig Model

Nutrients ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 749 ◽  
Author(s):  
Stine Hansen ◽  
Jane Jørgensen ◽  
Jens Nyengaard ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Synaptic Plasticity ◽  
Vitamin C ◽  
Guinea Pig ◽  
Early Life ◽  
Pyramidal Neurons ◽  
Pig Model ◽  
Vitamin C Deficiency ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Guinea Pig Model

scholarly journals Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains

Redox Biology ◽  
2014 ◽  
Vol 2 ◽  
pp. 361-367 ◽  
Author(s):  
Maya D. Paidi ◽  
Janne G. Schjoldager ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Guinea Pig ◽  
Late Gestation ◽  
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.

scholarly journals Vitamin C Deficiency and Scurvy Are Not Only a Dietary Problem but Are Codetermined by the Haptoglobin Polymorphism

2007 ◽  
Vol 53 (8) ◽  
pp. 1397-1400 ◽  
Author(s):  
Joris R Delanghe ◽  
Michel R Langlois ◽  
Marc L De Buyzere ◽  
Mathieu A Torck
Keyword(s):  
Vitamin C ◽  
Ldl Oxidation ◽  
Long Distance ◽  
Vitamin C Deficiency ◽  
Asian Populations ◽  
Functional Differences ◽  
Clinical Consequences ◽  
Genetically Determined

Abstract Ascorbic acid (vitamin C) is prone to oxidation in vivo. The human plasma protein haptoglobin (Hp) shows a genetic polymorphism with 3 major phenotypes (Hp 1-1, Hp 2-1, and Hp 2-2) that show important functional differences. Despite an adequate nutritional supply, in Hp 2-2 individuals (most common among Asian populations) vitamin C is markedly lower in concentration and particularly prone to oxidation in vivo. Therefore, susceptibility to subclinical and clinical vitamin C deficiency (scurvy) is partly genetically determined. The genetic advantage of the Hp1 allele as a vitamin C stabilizing factor helps to elucidate the direction and successes of long-distance sea crossing human migrations in history. Clinical trials demonstrated Hp phenotype–related effects of antioxidant treatment. Because vitamin C is a first line antioxidant, Hp polymorphism and its effects on vitamin C have major clinical consequences; a marked difference in genetic susceptibility toward atherosclerosis between Hp phenotypes is attributable to variation in LDL oxidation. The classical view of vitamin C and scurvy being a pure nutritional condition needs to be updated. These findings should foster research investigating the role of Hp polymorphism in human disease, and in vitamin C deficiency and atherosclerosis in particular.

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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