scholarly journals Liver Mitochondrial DNA Copy Number and Deletion Levels May Contribute to Nonalcoholic Fatty Liver Disease Susceptibility

2016 ◽  
Vol 16 (12) ◽  
Author(s):  
Sharareh Kamfar ◽  
Seyed Moayed Alavian ◽  
Massoud Houshmand ◽  
Reza Yadegarazari ◽  
Bahram Seifi Zarei ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Copy Number ◽  
Fatty Liver Disease ◽  
Disease Susceptibility ◽  
Dna Copy Number ◽  
Nonalcoholic Fatty Liver ◽  
Mitochondrial Dna Copy Number

scholarly journals Oxidative Stress and Nonalcoholic Fatty Liver Disease in Hemodialysis Patients

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Po-Jung Wu ◽  
Jin-Bor Chen ◽  
Wen-Chin Lee ◽  
Hwee-Yeong Ng ◽  
Shu-Ching Lien ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Cellulose Membrane ◽  
Nonalcoholic Fatty Liver ◽  
Factors Associated ◽  
Copy Numbers

Introduction. Nonalcoholic fatty liver disease (NAFLD) is becoming more common around the world and it may progress to cirrhosis and liver failure, increasing mortality risk. In hemodialysis (HD) patients, NAFLD may be a novel risk factor for their high cardiovascular mortality. Heightened oxidative stress is highly prevalent in HD patients. However, the relationship between oxidative stress and NAFLD in HD patients is not well defined.Methods. We studied seventy-one stable nondiabetic HD patients. Nineteen patients had the diagnosis of NAFLD by ultrasonography. Blood levels of oxidative stress markers were measured in each patient, including thiobarbituric acid reactive substances (TBARS), free thiols, superoxide dismutase (SOD) activities, and glutathione peroxidase (GPx) activity. The copy numbers of mitochondrial DNA (mtDNA) in peripheral leukocytes were also determined. Demographic, biochemistry, and hemogram data were recorded. The two groups of patients were compared in order to determine the factors associated with NAFLD in HD patients.Findings. Compared to those without NAFLD, nondiabetic HD patients with NAFLD had significantly higher mtDNA copy number and GPx levels. The two groups did not differ significantly in dialysis adequacy, hemoglobin, serum calcium, phosphorus, albumin, liver function tests, or lipid profiles. Regression analysis confirmed mtDNA copy numbers and GPx levels as two independent factors associated with NAFLD. Compared to those with polysulfone, patients dialyzed with cellulose membrane have significantly higher levels of TBARS. However, patients with or without NAFLD did not differ in their use of either dialysis membrane.Discussion. Oxidative stress (represented by antioxidant defense, GPx) and mitochondrial DNA copy numbers are independently associated with fatty liver disease in nondiabetic HD patients. The diagnostic and therapeutic implications of this key observation warrant further exploration.

578 OXIDATIVE DNA DAMAGE LEADING TO MITOCHONDRIAL DNA DEPLETION AGGRAVATES PEDIATRIC NONALCOHOLIC FATTY LIVER DISEASE (PNAFLD)

2021 ◽  
Vol 160 (6) ◽  
pp. S-113
Author(s):  
Preeti Viswanathan ◽  
Luka Maisuradze ◽  
Tatyana Tchaikovskaya ◽  
Bryan Rudolph ◽  
Michelle Ewart ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Oxidative Dna Damage ◽  
Nonalcoholic Fatty Liver ◽  
Mitochondrial Dna Depletion

Epigenetic modification of liver mitochondrial DNA is associated with histological severity of nonalcoholic fatty liver disease

Gut ◽  
2012 ◽  
Vol 62 (9) ◽  
pp. 1356-1363 ◽  
Author(s):  
Carlos Jose Pirola ◽  
Tomas Fernández Gianotti ◽  
Adriana Laura Burgueño ◽  
Manuel Rey-Funes ◽  
Cesar Fabian Loidl ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Epigenetic Modification ◽  
Nonalcoholic Fatty Liver

scholarly journals Peripheral blood mitochondrial DNA copy number, a potential marker of non‐alcoholic fatty liver disease?

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Maria Azucena Pescador Tapia ◽  
Nicolas Fragoso‐Bargas ◽  
Dalia Rodríguez‐Ríos ◽  
María Luisa Lazo‐de‐la‐Vega‐Monroy ◽  
Lorena Rocío Ibarra‐Reynoso ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Peripheral Blood ◽  
Copy Number ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Mitochondrial Dna Copy Number ◽  
Potential Marker ◽  
Alcoholic Fatty Liver Disease

Mitochondrial oxidative injury: a key player in nonalcoholic fatty liver disease

2020 ◽  
Vol 319 (3) ◽  
pp. G400-G411
Author(s):  
Waleska Dornas ◽  
Detlef Schuppan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dna ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Respiratory Chain ◽  
Fatty Liver Disease ◽  
Oxygen Species ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease worldwide. NAFLD is tightly linked to the metabolic syndrome, insulin resistance, and oxidative stress. Globally, its inflammatory form, nonalcoholic steatohepatitis (NASH), has become the main cause of liver-related morbidity and mortality, mainly due to liver cirrhosis and primary liver cancer. One hallmark of NASH is the presence of changes in mitochondrial morphology and function that are accompanied by a blocked flow of electrons in the respiratory chain, which increases formation of mitochondrial reactive oxygen species in a self-perpetuating vicious cycle. Consequences are oxidation of DNA bases and mitochondrial DNA depletion that are coupled with genetic and acquired mitochondrial DNA mutations, all impairing the resynthesis of respiratory chain polypeptides. In general, several maladaptations of pathways that usually maintain energy homeostasis occur with the early and late excess metabolic stress in NAFLD and NASH. We discuss the interplay between hepatocyte mitochondrial stress and inflammatory responses, focusing primarily on events initiated and maintained by mitochondrial free radical-induced damage in NAFLD. Importantly, mitochondrial oxidative stress and dysfunction are modulated by key pharmacological targets that are related to excess production of reactive oxygen species, mitochondrial turnover and the mitochondrial unfolded protein response, mitophagy, and mitochondrial biogenesis. However, the efficacy of such interventions depends on NAFLD/NASH disease stage.

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