scholarly journals The Role of Vitamin Deficiency in Liver Disease: To Supplement or Not Supplement?

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4014
Author(s):  
Anna Licata ◽  
Maddalena Zerbo ◽  
Silvia Como ◽  
Marcella Cammilleri ◽  
Maurizio Soresi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Tumors ◽  
Treatment Programs ◽  
Specific Knowledge ◽  
Nutritional Factors ◽  
Vitamin Deficiencies ◽  
Vitamin Intake ◽  
Poor Outcomes ◽  
The Impact

Over the past few years, growing interest has been shown for the impact of dietary requirements and nutritional factors on chronic diseases. As a result, nutritional programs have been reinforced by public health policies. The precise role of micronutrients in chronic liver disease is currently receiving particular attention since abnormalities in vitamin levels are often detected. At present, treatment programs are focused on correcting vitamin deficiencies, which are frequently correlated to higher rates of comorbidities with poor outcomes. The literature reviewed here indicates that liver diseases are often related to vitamin disorders, due to both liver impairment and abnormal intake. More specific knowledge about the role of vitamins in liver disease is currently emerging from various results and recent evidence. The most significant benefits in this area may be observed when improved vitamin intake is combined with a pharmacological treatment that may also affect the progression of the liver disease, especially in the case of liver tumors. However, further studies are needed.

scholarly journals Role of autophagy in the pathogenesis of liver diseases

2011 ◽  
Vol 152 (49) ◽  
pp. 1955-1961 ◽  
Author(s):  
Klára Werling
Keyword(s):  
Endoplasmic Reticulum ◽  
Liver Disease ◽  
Liver Diseases ◽  
Liver Tumors ◽  
Liver Steatosis ◽  
Prognostic Significance ◽  
Adenosine Monophosphate ◽  
Mutant Proteins ◽  
Alpha 1 Antitrypsin Deficiency

Autophagy is a self-digestion process that plays an important role in the development, differentiation and homeostasis of cells, helping their survival during starvation and hypoxia. Accumulated mutant proteins in the endoplasmic reticulum can be degraded by autophagy in alpha-1 antitrypsin deficiency. Hepatitis C and B virus may exploit the autophagy pathway to escape the innate immune response and to promote their own replication. Autophagy is decreased in response to chronic alcohol consumption, likely due to a decrease in 5’-adenosine monophosphate-activated protein kinase, increase in mTOR activity and due to an alteration in vesicle transport in hepatocytes. In obesity and alcoholic liver disease the decreased function of autophagy causes formation of Mallory-Denk bodies and cell death. The deficient autophagy can contribute to liver steatosis, to endoplasmic reticulum stress, and to progression of liver disease. Autophagy defect in hepatocellular carcinoma suggests that it can serve a tumor-suppressor function. The autophagy protein Beclin-1 levels have prognostic significance in liver tumors. Understanding of the molecular mechanism and the role of autophagy may lead to more effective therapeutic strategies in liver diseases in the future. Orv. Hetil., 2011, 152, 1955–1961.

scholarly journals TET2 mutations as a part of DNA dioxygenase deficiency in myelodysplastic syndromes

2021 ◽  
Author(s):  
Carmelo Gurnari ◽  
Simona Pagliuca ◽  
Yihong Guan ◽  
Vera Adema ◽  
Courtney E Hershberger ◽  
...  
Keyword(s):  
Myelodysplastic Syndromes ◽  
Prognostic Significance ◽  
Age Groups ◽  
Feedback Mechanism ◽  
Dna Demethylation ◽  
Compensatory Mechanisms ◽  
Poor Outcomes ◽  
Relationship Of ◽  
The Impact

Decrease in DNA dioxygease activity generated by TET2 gene family is crucial in myelodysplastic syndromes (MDS). The general down-regulation of 5-hydroxymethylcytosine (5-hmC) argues for a role of DNA demethylation in MDS beyond TET2 mutations, which albeit frequent, do not convey any prognostic significance. We investigated TETs expression to identify factors which can modulate the impact of mutations and thus 5-hmC levels on clinical phenotypes and prognosis of MDS patients. DNA/RNA-sequencing and 5-hmC data were collected from 1,665 patients with MDS and 91 controls. Irrespective of mutations, a significant fraction of MDS patients exhibited lower TET2 expression, while 5-hmC levels were not uniformly decreased. In searching for factors explaining compensatory mechanisms, we discovered that TET3 was up-regulated in MDS and inversely correlated with TET2 expression in wild-type cases. While TET2 was reduced across all age-groups, TET3 levels were increased in a likely feedback mechanism induced by TET2 dysfunction. This inverse relationship of TET2 and TET3 expression also corresponded to the expression of L-2-hydroxyglutarate dehydrogenase, involved in agonist/antagonist substrate metabolism. Importantly, elevated TET3 levels influenced the clinical phenotype of TET2-deficiency whereby the lack of compensation by TET3 (low TET3 expression) was associated with poor outcomes of TET2 mutant carriers.

scholarly journals Up-Regulated MicroRNA-27b Promotes Adipocyte Differentiation via Induction of Acyl-CoA Thioesterase 2 Expression

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Yuka Murata ◽  
Takashi Yamashiro ◽  
Takaomi Kessoku ◽  
Israt Jahan ◽  
Haruki Usuda ◽  
...  
Keyword(s):  
Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Adipocyte Differentiation ◽  
Aberrant Expression ◽  
Nonalcoholic Fatty Liver ◽  
Important Pathway ◽  
The Impact ◽  
Intracellular Triglyceride

Nonalcoholic fatty liver disease (NAFLD) is characterized by a spectrum of liver pathologies, from simple steatosis to steatohepatitis. Recent studies have increasingly noted the aberrant expression of microRNAs closely related to NAFLD pathologies. We have previously shown the presence of increased levels of microRNA-27b (miR-27b) in patients with NAFLD. In this study, we investigated the role of miR-27b in NAFLD by examining the impact of up-regulated miR-27b on the differentiation of preadipocytes into mature adipocytes. We found that miR-27b-3p remarkably enhances the adipocyte differentiation of 3T3-L1 cells associated with lipid accumulation and intracellular triglyceride contents. Furthermore, we have demonstrated not only that miR-27b-3p induces acyl-CoA thioesterase 2 (ACOT2) expression in 3T3-L1 cells, but also that the knockdown of ACOT2 suppresses lipid accumulation and adipocyte differentiation in both the presence and absence of miR-27b-3p treatment. Our data strongly suggest that the miR-27b-ACOT2 axis is an important pathway in adipocyte differentiation and may play a role in the pathogenesis of NAFLD.

scholarly journals Emerging role of circadian clock disruption in alcohol-induced liver disease

2018 ◽  
Vol 315 (3) ◽  
pp. G364-G373 ◽  
Author(s):  
Shannon M. Bailey
Keyword(s):  
Liver Disease ◽  
Circadian Clock ◽  
Therapeutic Approaches ◽  
Excessive Alcohol Consumption ◽  
Peripheral Tissues ◽  
New Therapeutic Approaches ◽  
Timing System ◽  
Excessive Alcohol ◽  
The Impact

The detrimental health effects of excessive alcohol consumption are well documented. Alcohol-induced liver disease (ALD) is the leading cause of death from chronic alcohol use. As with many diseases, the etiology of ALD is influenced by how the liver responds to other secondary insults. The molecular circadian clock is an intrinsic cellular timing system that helps organisms adapt and synchronize metabolism to changes in their environment. The clock also influences how tissues respond to toxic, environmental, and metabolic stressors, like alcohol. Consistent with the essential role for clocks in maintaining health, genetic and environmental disruption of the circadian clock contributes to disease. While a large amount of rich literature is available showing that alcohol disrupts circadian-driven behaviors and that circadian clock disruption increases alcohol drinking and preference, very little is known about the role circadian clocks play in alcohol-induced tissue injuries. In this review, recent studies examining the effect alcohol has on the circadian clock in peripheral tissues (liver and intestine) and the impact circadian clock disruption has on development of ALD are presented. This review also highlights some of the rhythmic metabolic processes in the liver that are disrupted by alcohol and potential mechanisms through which alcohol disrupts the liver clock. Improved understanding of the mechanistic links between the circadian clock and alcohol will hopefully lead to the development of new therapeutic approaches for treating ALD and other alcohol-related organ pathologies.

scholarly journals Role of Hepatitis E Virus Infection in Acute-on-Chronic Liver Failure

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Mario Frias ◽  
Pedro López-López ◽  
Antonio Rivero ◽  
Antonio Rivero-Juarez
Keyword(s):  
Liver Disease ◽  
Liver Failure ◽  
Hepatitis E Virus ◽  
Hepatitis E ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Hepatic Decompensation ◽  
End Stage ◽  
The Impact

Chronic liver disease (CLD) with a variety of causes is currently reported to be one of the main causes of death worldwide. Patients with CLD experience deteriorating liver function and fibrosis, progressing to cirrhosis, chronic hepatic decompensation (CHD), end-stage liver disease (ESLD), and death. Patients may develop acute-on-chronic liver failure (ACLF), typically related to a precipitating event and associated with increased mortality. The objective of this review was to analyze the role of acute hepatitis E virus (HEV) infection in patients with CLD, focusing on the impact of this infection on patient survival and prognosis in several world regions.

scholarly journals The impact of PNPLA3 and TM6SF2 in cirrhosis related complications

2021 ◽  
Author(s):  
Haruki Uojima ◽  
Xue Shao ◽  
Taeang Arai ◽  
Yuji ogawa ◽  
Toru Setsu ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Odds Ratio ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Fibrosis Progression ◽  
Cirrhotic Patients ◽  
The Impact

Patatin-like phospholipase domain-containing 3 (PNPLA3) and transmembrane 6-superfamily member 2 (TM6SF2) polymorphisms have major impact for fibrosis due to steatohepatitis. However, there are scant data about correlations between cirrhosis-related complications and the polymorphisms of these genes. Therefore, we aimed to determine the role of the PNPLA3 and TM6SF2 polymorphisms in fibrosis progression for patients with liver cirrhosis. A multicenter study was performed at six hospitals in Japan enrolling 400 patients with liver cirrhosis caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33). These cirrhotic patients included those with complications of variceal bleeding, hepatic ascites, and/or hepatic encephalopathy and those without. To assess the role of the PNPLA3 and TM6SF2 polymorphisms in patients with cirrhosis related complications, we calculated the odds ratio and relative risk for the rs738409 and rs58542926 polymorphisms. We also accessed whether or not the interaction between these two polymorphisms contributed to cirrhosis related complications. As a result, the odds ratio for complications in the NAFLD group significantly increased in the presence of the rs738409 GG genotype when the CC genotype was used as the reference. There were no significant risks between complications and the presence of the rs738409 G allele in the virus or alcohol groups. There were no significant risks of complications in the frequency of the rs58542926 T polymorphism regardless of the etiology of liver cirrhosis. The interaction between the trs738409 and rs58542926 polymorphisms had the highest odds ratio of 2.415 for complications in the rs738409 GG + rs58542926 (CT+TT) group when rs738409 (CC+CG) + TM6SF2 CC was used as the reference in the NAFLD group.

scholarly journals Pathogenesis of Ischemic Stroke: Role of Epigenetic Mechanisms

Genes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 89 ◽  
Author(s):  
Rosita Stanzione ◽  
Maria Cotugno ◽  
Franca Bianchi ◽  
Simona Marchitti ◽  
Maurizio Forte ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Epigenetic Modifications ◽  
Review Article ◽  
Epigenetic Changes ◽  
Therapeutic Approaches ◽  
Nutritional Factors ◽  
New Therapeutic Approaches ◽  
Different Types ◽  
The Impact

Epigenetics is the branch of molecular biology that studies modifications able to change gene expression without altering the DNA sequence. Epigenetic modulations include DNA methylation, histone modifications, and noncoding RNAs. These gene modifications are heritable and modifiable and can be triggered by lifestyle and nutritional factors. In recent years, epigenetic changes have been associated with the pathogenesis of several diseases such as diabetes, obesity, renal pathology, and different types of cancer. They have also been related with the pathogenesis of cardiovascular diseases including ischemic stroke. Importantly, since epigenetic modifications are reversible processes they could assist with the development of new therapeutic approaches for the treatment of human diseases. In the present review article, we aim to collect the most recent evidence concerning the impact of epigenetic modifications on the pathogenesis of ischemic stroke in both animal models and humans.

scholarly journals Later School Start Time: The Impact of Sleep on Academic Performance and Health in the Adolescent Population

2020 ◽  
Vol 17 (7) ◽  
pp. 2574 ◽  
Author(s):  
Valentina Alfonsi ◽  
Serena Scarpelli ◽  
Aurora D’Atri ◽  
Giacomo Stella ◽  
Luigi De Gennaro
Keyword(s):  
Learning Ability ◽  
Treatment Programs ◽  
Physical And Mental Health ◽  
Sleep Patterns ◽  
Start Time ◽  
Impaired Sleep ◽  
The Impact ◽  
The Relationship ◽  
Chronic Sleep

The crucial role of sleep in physical and mental health is well known, especially during the developmental period. In recent years, there has been a growing interest in examining the relationship between sleep patterns and school performance in adolescents. At this stage of life, several environmental and biological factors may affect both circadian and homeostatic regulation of sleep. A large part of this population does not experience adequate sleep, leading to chronic sleep restriction and/or disrupted sleep–wake cycles. Studies investigating the effects of different sleep–wake schedules on academic achievement showed that impaired sleep quality and quantity are associated with decreased learning ability and compromised daytime functioning. This review focuses on the most recent studies that evaluated the effects of modified school start time on sleep patterns and related outcomes. Moreover, based on the available empirical evidence, we intend to propose a direction for future studies targeted to implement prevention or treatment programs by modifying sleep timing.

Non-Alcoholic Fatty Liver Disease and Vascular Disease

2020 ◽  
Vol 19 (3) ◽  
pp. 269-279
Author(s):  
Roberta Forlano ◽  
Benjamin H. Mullish ◽  
Rooshi Nathwani ◽  
Ameet Dhar ◽  
Mark R. Thursz ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
High Risk Population ◽  
Younger Adults ◽  
Alcoholic Fatty Liver ◽  
Emerging Risk ◽  
The Impact ◽  
Alcoholic Fatty Liver Disease

Non-Alcoholic Fatty Liver Disease (NAFLD) represents an increasing cause of liver disease worldwide. However, notably, the primary cause of morbidity and mortality in patients with NAFLD is cardiovascular disease (CVD), with fibrosis stage being the strongest disease-specific predictor. It is globally projected that NAFLD will become increasingly prevalent, especially among children and younger adults. As such, even within the next few years, NAFLD will contribute considerably to the overall CVD burden. In this review, we discuss the role of NAFLD as an emerging risk factor for CVD. In particular, this article aims to provide an overview of pathological drivers of vascular damage in patients with NAFLD. Moreover, the impact of NAFLD on the development, severity and the progression of subclinical and clinical CVD will be discussed. Finally, the review illustrates current and potential future perspectives to screen for CVD in this high-risk population.

scholarly journals Genomics of Viral Hepatitis-Associated Liver Tumors

2021 ◽  
Vol 10 (9) ◽  
pp. 1827
Author(s):  
Camille Péneau ◽  
Jessica Zucman-Rossi ◽  
Jean-Charles Nault
Keyword(s):  
Hepatitis B ◽  
Insertional Mutagenesis ◽  
Liver Tumors ◽  
Tumor Development ◽  
Driver Genes ◽  
Adeno Associated Virus ◽  
Cancer Driver ◽  
B Virus ◽  
The Impact

Virus-related liver carcinogenesis is one of the main contributors of cancer-related death worldwide mainly due to the impact of chronic hepatitis B and C infections. Three mechanisms have been proposed to explain the oncogenic properties of hepatitis B virus (HBV) infection: induction of chronic inflammation and cirrhosis, expression of HBV oncogenic proteins, and insertional mutagenesis into the genome of infected hepatocytes. Hepatitis B insertional mutagenesis modifies the function of cancer driver genes and could promote chromosomal instability. In contrast, hepatitis C virus promotes hepatocellular carcinoma (HCC) occurrence mainly through cirrhosis development whereas the direct oncogenic role of the virus in human remains debated. Finally, adeno associated virus type 2 (AAV2), a defective DNA virus, has been associated with occurrence of HCC harboring insertional mutagenesis of the virus. Since these tumors developed in a non-cirrhotic context and in the absence of a known etiological factor, AAV2 appears to be the direct cause of tumor development in these patients via a mechanism of insertional mutagenesis altering similar oncogenes and tumor suppressor genes targeted by HBV. A better understanding of virus-related oncogenesis will be helpful to develop new preventive strategies and therapies directed against specific alterations observed in virus-related HCC.

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