The role of adipocyte fatty acid binding protein in the pathogenesis of non-alcoholic fatty liver disease

2010 ◽  
Author(s):  
Yue-ling Wong
2013 ◽  
Vol 26 (3) ◽  
pp. 241-247 ◽  
Author(s):  
Marco Masetti ◽  
Giampaolo Bianchi ◽  
Giordano Gianotti ◽  
Marco Giovagnoli ◽  
Luca Vizioli ◽  
...  

2019 ◽  
Vol 09 (06) ◽  
pp. 113-124
Author(s):  
Badawy A. Abdulaziz ◽  
Sabry Anis Abdu ◽  
Ahmed Mostafa Amin ◽  
Ahmed Khayri Abdel Hamid El Menyawi ◽  
Abdelmoneam Ahmed ◽  
...  

2014 ◽  
Vol 128 (1-2) ◽  
pp. 48-52 ◽  
Author(s):  
Erdem Akbal ◽  
Erdem Koçak ◽  
Ömer Akyürek ◽  
Seyfettin Köklü ◽  
Hikmetullah Batgi ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Ricardo Rodríguez-Calvo ◽  
Juan Moreno-Vedia ◽  
Josefa Girona ◽  
Daiana Ibarretxe ◽  
Neus Martínez-Micaelo ◽  
...  

Background: Liver steatosis is considered the onset of the non-alcoholic fatty liver disease (NAFLD), a major public health challenge. Nevertheless, NAFLD detection and diagnosis remain a difficult task. Fatty acid binding protein 4 (FABP4) has been proposed as potential biomarker for the ectopic fat accumulation in non-adipose tissues, although its role reflecting liver steatosis in metabolic patients is not fully explored. The aim of this study was to assess the relationship between FABP4 and the fatty liver index (FLI) in metabolic patients and to evaluate its potential role in the fatty liver disease.Methods: A cross-sectional study involving 389 participants at increased cardiometabolic risk was performed. FLI was calculated in order to assess liver fatty disease and a FLI ≥ 60 was considered to define liver steatosis. The serum FABP4 levels were assessed by using a sandwich enzyme-linked immunosorbent assay. Multivariable regression models were used to examine the associations of FABP4 with fatty liver after adjusting for demographic and clinical characteristics.Results: Both, FLI and serum FABP4 levels were upregulated in diabetic, obese, and metabolic syndrome patients. Serum FABP4 levels were higher in individuals with liver steatosis. Serum FABP4 were robustly associated with FLI in metabolic patients in both linear and logistic regression analyses.Conclusion: Our findings show that the serum FABP4 is associated to liver steatosis in metabolic patients.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Arezoo Gowhari Shabgah ◽  
Fatemeh Norouzi ◽  
Mahdiyeh Hedayati-Moghadam ◽  
Davood Soleimani ◽  
Naseh Pahlavani ◽  
...  

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.


2021 ◽  
Vol 11 ◽  
Author(s):  
Aldo Grefhorst ◽  
Ivo P. van de Peppel ◽  
Lars E. Larsen ◽  
Johan W. Jonker ◽  
Adriaan G. Holleboom

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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