Journal ArticleDOI
Redox balance in the pathogenesis of nonalcoholic fatty liver disease: mechanisms and therapeutic opportunities.
TLDR
Intacellular mechanisms, including mitochondrial dysfunction and impaired oxidative free fatty acid metabolism, leading to reactive oxygen species generation, and the potential pathogenetic role of extracellular sources of reactive oxygen Species in NAFLD, including increased myeloperoxidase activity and oxidized low density lipoprotein accumulation, will be reviewed.Abstract:
Nonalcoholic fatty liver disease (NAFLD) is currently the most common liver disease in the world. It encompasses a histological spectrum, ranging from simple, nonprogressive steatosis to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis and hepatocellular carcinoma. While liver-related complications are confined to NASH, emerging evidence suggests both simple steatosis and NASH predispose to type 2 diabetes and cardiovascular disease. The pathogenesis of NAFLD is currently unknown, but accumulating data suggest that oxidative stress and altered redox balance play a crucial role in the pathogenesis of steatosis, steatohepatitis, and fibrosis. We will examine intracellular mechanisms, including mitochondrial dysfunction and impaired oxidative free fatty acid metabolism, leading to reactive oxygen species generation; additionally, the potential pathogenetic role of extracellular sources of reactive oxygen species in NAFLD, including increased myeloperoxidase activity and oxidized ...read more
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Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials
TL;DR: Weight loss is safe, and improves liver histology and cardio-metabolic profile, and for patients not responding to lifestyle intervention, pioglitazone improves histological disease activity, slows fibrosis progression and extensively ameliorates cardio- Metabolic endpoints.
Journal ArticleDOI
The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Konstantin Kazankov,Simon Mark Dahl Jørgensen,Karen Louise Thomsen,Holger Jon Møller,Hendrik Vilstrup,Jacob George,Detlef Schuppan,Detlef Schuppan,Henning Grønbæk +8 more
TL;DR: Experimental and clinical data support a central role for macrophages in the development and progression of nonalcoholic fatty liver disease (NAFLD) and non alcoholic steatohepatitis (NASH) and studies investigating drugs that target macrophage recruitment to the liver, Macrophage polarization and their inflammatory effects as potential treatment options for patients with NASH are reviewed.
Journal ArticleDOI
An Integrated Understanding of the Rapid Metabolic Benefits of a Carbohydrate-Restricted Diet on Hepatic Steatosis in Humans
Adil Mardinoglu,Hao Wu,Elias Björnson,Cheng Zhang,Antti Hakkarainen,Sari M. Räsänen,Sunjae Lee,Rosellina Margherita Mancina,Mattias Bergentall,Kirsi H. Pietiläinen,Sanni Söderlund,Niina Matikainen,Marcus Ståhlman,Per Olof Bergh,Martin Adiels,Brian D. Piening,Marit Granér,Nina Lundbom,Kevin Jon Williams,Stefano Romeo,Jens Nielsen,Michael Snyder,Mathias Uhlén,Göran Bergström,Rosie Perkins,Hanns-Ulrich Marschall,Fredrik Bäckhed,Marja-Riitta Taskinen,Jan Borén +28 more
TL;DR: A short-term intervention with an isocaloric low-carbohydrate diet with increased protein content in obese subjects with NAFLD and the resulting alterations in metabolism and the gut microbiota are characterized using a multi-omics approach to highlight the potential of exploring diet-microbiota interactions for treatingNAFLD.
Journal ArticleDOI
Fructose metabolism in humans – what isotopic tracer studies tell us
Sam Z. Sun,Mark Empie +1 more
TL;DR: The reviewed data provides a profile of how dietary fructose is utilized in humans and indicates that approximately a quarter of ingested fructose can be converted into lactate within a few of hours.
Journal ArticleDOI
Oxidative Stress as a Critical Factor in Nonalcoholic Fatty Liver Disease Pathogenesis
TL;DR: Although augmented concentrations of ROS and faulty antioxidant defense have been associated to NAFLD and related complications, mechanisms of action and proofs of principle should be highlighted to support the causative role of OxS and to translate its concept into the clinic.
References
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