Introduction to the special issue on role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease

Alcohol ◽  
2004 ◽  
Vol 34 (1) ◽  
pp. 1 ◽  
Author(s):  
Thomas R. Jerrells
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Alcoholic Liver Disease ◽  
Dietary Fatty Acid ◽  
Special Issue

scholarly journals The Role of TM6SF2 in Non-Alcoholic Fatty Liver Disease: From Mechanisms To Therapeutic Strategy

2021 ◽  
Author(s):  
Zuyin Li ◽  
Gang Wu ◽  
Chen Qiu ◽  
Zhijie Zhou ◽  
Yupeng Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Acid Metabolism ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Acid Metabolism ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract Background and aims : Lack of effective pharmacotherapies for nonalcoholic fatty liver disease (NAFLD) is mainly attributed to an insufficient research on its pathogenesis. In this paper, we investigated the role of TM6SF2 on fatty acid metabolism in the background of fatty liver, and proposed the possible therapeutic strategies of NAFLD caused by TM6SF2 deficiency. Methods Liver samples collected from both NAFLD mouse models and human subjects, and RNA-seq data retrieved from GEO database were used to evaluate the expression of TM6SF2 in NAFLD. Knockdown of TM6SF2 was performed for clarifying the mechanistic basis of hepatic lipid accumulation in NAFLD. After confirming that TM6SF2 deficiency would cause an abnormality in fatty acid metabolism, MK-4074 administration served as the therapeutic intervention to evaluate its effect on NAFLD caused by TM6SF2 deficiency. Results Hepatic TM6SF2 levels are elevated in both NAFLD patients and mouse NAFLD models. In vivo and in vitro experiments confirmed that TM6SF2 knockdown increases intracellular lipid deposition due to dysregulated fatty acid metabolism in the context of TM6SF2 deficiency, being characterized by enhanced fatty acid uptake and synthesis, accompanied by impaired fatty acid oxidation. Moreover, MK-4074 treatment could reverse the NAFLD phenotypes caused by TM6SF2 deficiency. Conclusions TM6SF2 deficiency enhanced hepatic lipid accumulation through dysregulated fatty acid metabolism and MK-4074 treatment could alleviate the NAFLD phenotypes caused by TM6SF2 deficiency.

scholarly journals A comprehensive review of long non-coding RNAs in the pathogenesis and development of non-alcoholic fatty liver disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Arezoo Gowhari Shabgah ◽  
Fatemeh Norouzi ◽  
Mahdiyeh Hedayati-Moghadam ◽  
Davood Soleimani ◽  
Naseh Pahlavani ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Lipoprotein Metabolism ◽  
Alcoholic Fatty Liver ◽  
Fatty Acids Metabolism ◽  
Non Coding Rnas ◽  
Alcoholic Fatty Liver Disease

AbstractOne of the most prevalent diseases worldwide without a fully-known mechanism is non-alcoholic fatty liver disease (NAFLD). Recently, long non-coding RNAs (lncRNAs) have emerged as significant regulatory molecules. These RNAs have been claimed by bioinformatic research that is involved in biologic processes, including cell cycle, transcription factor regulation, fatty acids metabolism, and-so-forth. There is a body of evidence that lncRNAs have a pivotal role in triglyceride, cholesterol, and lipoprotein metabolism. Moreover, lncRNAs by up- or down-regulation of the downstream molecules in fatty acid metabolism may determine the fatty acid deposition in the liver. Therefore, lncRNAs have attracted considerable interest in NAFLD pathology and research. In this review, we provide all of the lncRNAs and their possible mechanisms which have been introduced up to now. It is hoped that this study would provide deep insight into the role of lncRNAs in NAFLD to recognize the better molecular targets for therapy.

The Role of Visceral Adipose Tissue in the Pathogenesis of Non-alcoholic Fatty Liver Disease

2010 ◽  
Vol 7 (2) ◽  
pp. 96 ◽  
Author(s):  
An Verrijken ◽  
Sven Francque ◽  
Luc Van Gaal ◽  
◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Visceral Adipose ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD), the most common cause of chronic liver disease in Western countries, comprises a disease spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), advanced fibrosis and cirrhosis. Fatty liver develops when fatty acid uptake and de novo fatty acid synthesis exceed fatty acid oxidation and export as very low-density lipoprotein/triglycerides. Because of its high prevalence and its association with obesity, metabolic syndrome, type 2 diabetes, dyslipidaemia and hypertension, NAFLD has become an important public health problem. The pathogenesis of NAFLD has to date not been completely clarified. Research has been conducted regarding the role of insulin resistance, lipotoxicity, oxidative stress and chronic inflammation. Visceral adipose tissue has increasingly been recognised as a biologically active organ contributing to the pathogenesis of NAFLD. Its role in the development of fatty liver might be situated at several levels: as a source of free fatty acids, by the production of adipocytokines, as a cause of insulin resistance and by inflammation.

scholarly journals The Role of Lipophagy in the Development and Treatment of Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol 11 ◽  
Author(s):  
Aldo Grefhorst ◽  
Ivo P. van de Peppel ◽  
Lars E. Larsen ◽  
Johan W. Jonker ◽  
Adriaan G. Holleboom
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Lipid Homeostasis ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Triglyceride Accumulation ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) or metabolic (dysfunction) associated liver disease (MAFLD), is, with a global prevalence of 25%, the most common liver disorder worldwide. NAFLD comprises a spectrum of liver disorders ranging from simple steatosis to steatohepatitis, fibrosis, cirrhosis and eventually end-stage liver disease. The cause of NAFLD is multifactorial with genetic susceptibility and an unhealthy lifestyle playing a crucial role in its development. Disrupted hepatic lipid homeostasis resulting in hepatic triglyceride accumulation is an hallmark of NAFLD. This disruption is commonly described based on four pathways concerning 1) increased fatty acid influx, 2) increased de novo lipogenesis, 3) reduced triglyceride secretion, and 4) reduced fatty acid oxidation. More recently, lipophagy has also emerged as pathway affecting NAFLD development and progression. Lipophagy is a form of autophagy (i.e. controlled autolysosomal degradation and recycling of cellular components), that controls the breakdown of lipid droplets in the liver. Here we address the role of hepatic lipid homeostasis in NAFLD and specifically review the current literature on lipophagy, describing its underlying mechanism, its role in pathophysiology and its potential as a therapeutic target.

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