Abstract
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.
Highlights
Redox imbalance and consequent oxidative stress is an important driver of hepatocellular damage in non-alcoholic fatty liver disease (NAFLD) and the subsequent progression to steaotohepatitis (NASH) and fibrosis; a primary indicator for liver transplantation [1,2].A causal connection to a chronically high calorie intake combined with a sedentary lifestyle ties NAFLD to the broadly termed “lifestyle associated diseases”, hereby representing the hepatic consequence of metabolic dysfunction [3,4]
This study investigated the potential burden of vitamin C deficiency—often resulting from a poor diet low in fruits and vegetables and high in fat—on the guinea pig NAFLD/NASH phenotype and hepatic transcriptome
While there were no differences in body weights in the pre-intervention period, Figure 3A shows a clear effect of diet (p < 0.01) in the post-intervention period and no effect of vitamin C (vitC)
Summary
A causal connection to a chronically high calorie intake (in the form of fat, cholesterol, and sugars) combined with a sedentary lifestyle ties NAFLD to the broadly termed “lifestyle associated diseases”, hereby representing the hepatic consequence of metabolic dysfunction [3,4]. In this way, closely linked to dyslipidemia and metabolic stress, an imposing state of redox imbalance and resulting oxidative stress in NAFLD induces hepatocellular damage and release of inflammatory cytokines and profibrotic factors, driving disease progression with serious consequences for liver function and patient health [2,5]. Though mechanisms are not completely disclosed, vitE has been included as part of the treatment guidelines for some NAFLD patients [12,13,14,15,16]
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