Vitamin D supplementation in patients with alcoholic liver cirrhosis: a prospective study

Savić, Željka; Vračarić, Vladimir; Milić, Nataša; Nićiforović, Dijana; Damjanov, Dragomir; Pellicano, Rinaldo; Medić-Stojanoska, Milica; Abenavoli, Ludovico

doi:10.23736/s0026-4806.18.05723-3

Cited by 30 publications

(13 citation statements)

References 22 publications

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“…A clinical study found that low 25(OH)D levels were associated with increased mortality in ALD [12]. Another prospective study found that supplementation with vitamin D reduced the Child-Pugh score in patients with alcoholic liver cirrhosis [13]. Increasing data demonstrate that vitamin D has an antioxidant activity [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Chu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Vitamin D deficiency has been reported in alcoholics. This study is aimed at evaluating the effects of vitamin D deficiency on chronic alcohol-induced liver injury in mice. Mice were fed with modified Lieber-DeCarli liquid diets for 6 weeks to establish an animal model of chronic alcohol-induced liver injury. In the VDD+EtOH group, mice were fed with modified diets, in which vitamin D was depleted. Vitamin D deficiency aggravated alcohol-induced liver injury. Furthermore, vitamin D deficiency aggravated hepatocyte apoptosis during alcohol-induced liver injury. Although it has a little effect on hepatic TG content, vitamin D deficiency promoted alcohol-induced hepatic GSH depletion and lipid peroxidation. Further analysis showed that vitamin D deficiency further increased alcohol-induced upregulation of hepatic inducible nitric oxide synthase (inos), two NADPH oxidase subunits p47phox and gp91phox, and heme oxygenase- (HO-) 1. By contrast, vitamin D deficiency attenuated alcohol-induced upregulation of hepatic antioxidant enzyme genes, such as superoxide dismutase (sod) 1 and gshpx. In addition, vitamin D deficiency significantly elevated alcohol-induced upregulation of hepatic proinflammatory cytokines and chemokines. Taken together, these results suggest that vitamin D deficiency aggravates hepatic oxidative stress and inflammation during chronic alcohol-induced liver injury.

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Section: Introductionmentioning

confidence: 99%

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Chu

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…A recent transversal study in a cohort of alcoholic patients has observed that a severe deficiency in 25(OH)D is independently associated with the occurrence of alcoholic steatohepatitis (Anty et al, ). Another prospective study found that supplementation of vitamin D in patients with alcoholic liver cirrhosis for a period of at least 6 months decreases the Child‐Pugh score (Savic et al, ). Moreover, several studies have also report that low serum 1,25(OH) 2 D 3 levels are associated with a higher body mass index (BMI) and body fat mass in healthy adults (Kayaniyil et al, ; Parikh et al, ).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Deficiency Attenuates Acute Alcohol‐Induced Hepatic Lipid Accumulation in Mice

Yang

et al. 2019

Lipids

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Vitamin D deficiency has been frequently reported in chronic liver disease. However, its influence on hepatic lipid accumulation in alcoholic liver disease remains unclear. The present study investigated the effects of vitamin D deficiency on acute alcohol‐induced hepatic lipid metabolism in mice. Mice were fed with vitamin D deficient diet, in which vitamin D was depleted for 12 weeks to establish an animal model of vitamin D deficiency. Some mice were administered a single gavage of alcohol (4 g/kg bodyweight) before they were euthanized. Results show that feeding mice with vitamin D deficient diet did not induce hepatic lipid accumulation. In contrast, vitamin D deficiency markedly reduced alcohol‐induced triacylglycerol (TAG) content and prevented hepatic lipid accumulation. Moreover, vitamin D deficiency significantly attenuated alcohol‐induced sterol‐regulated element‐binding protein (SREBP)‐1c activation, which regulates genes for hepatic fatty acid (FA) and TAG synthesis, and the expression of its target genes fatty acid synthase (Fasn) and acetyl‐coenzyme‐ A carboxylase (Acc). In addition, vitamin D deficiency alleviated alcohol‐induced downregulation of hepatic nuclear peroxisome proliferator‐activated receptor (PPAR)α, which governs FA transport and β‐oxidation, and the expression of Carnitine palmitoyltransferase (Cpt)‐1α, cytochrome P450, family 4, subfamily a, polypeptide (Cyp4a)10, and Cyp4a14, which are key enzymes for hepatic fatty acids β‐oxidation and ω‐oxidation. Taken together, these results suggest that vitamin D deficiency is not a direct risk factor for hepatic lipid accumulation. Vitamin D deficiency alleviates acute alcohol‐induced hepatic lipid accumulation through inhibiting hepatic de novo fatty acid syntheses and promoting fatty acid β‐oxidation and ω‐oxidation.

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“…This study also found that vitamin D treatment or supplementation could suppress the expression of the pro-inflammatory cytokine TNFα, which further confirmed the role of vitamin D in immunomodulation. Moreover, the results of a prospective study among patients with alcoholic liver cirrhosis found that oral vitamin D supplementation decreased the Child-Pugh score and ameliorated liver damage[ 74 ]. Collectively, these data highlight the possibility that vitamin D may serve as a diagnostic biomarker and a potent agent in the management of ALD.…”

Section: Vitamin Metabolism In Aldmentioning

confidence: 99%

Current understanding of the metabolism of micronutrients in chronic alcoholic liver disease

Meng

2020

WJG

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Alcoholic liver disease (ALD) remains an important health problem worldwide. Perturbation of micronutrients has been broadly reported to be a common characteristic in patients with ALD, given the fact that micronutrients often act as composition or coenzymes of many biochemical enzymes responsible for the inflammatory response, oxidative stress, and cell proliferation. Mapping the metabolic pattern and the function of these micronutrients is a prerequisite before targeted intervention can be delivered in clinical practice. Recent years have registered a significant improvement in our understanding of the role of micronutrients on the pathogenesis and progression of ALD. However, how and to what extent these micronutrients are involved in the pathophysiology of ALD remains largely unknown. In the current study, we provide a review of recent studies that investigated the imbalance of micronutrients in patients with ALD with a focus on zinc, iron, copper, magnesium, selenium, vitamin D and vitamin E, and determine how disturbances in micronutrients relates to the pathophysiology of ALD. Overall, zinc, selenium, vitamin D, and vitamin E uniformly exhibited a deficiency, and iron demonstrated an elevated trend. While for copper, both an elevation and deficiency were observed from existing literature. More importantly, we also highlight several challenges in terms of low sample size, study design discrepancies, sample heterogeneity across studies, and the use of machine learning approaches.

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Vitamin D supplementation in patients with alcoholic liver cirrhosis: a prospective study

Cited by 30 publications

References 22 publications

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice

Vitamin D Deficiency Attenuates Acute Alcohol‐Induced Hepatic Lipid Accumulation in Mice

Current understanding of the metabolism of micronutrients in chronic alcoholic liver disease

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