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Raquel Barbuio, Marciane Milanski, Manoel B Bertolo, Mário J Saad, and Lício A Velloso

Introduction Non-alcoholic fatty liver disease (NAFLD) comprehends a large spectrum of clinicopathological conditions of the liver, ranging from steatosis to cirrhosis, and including steatohepatitis (NASH) and fibrosis ( Browning

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Flávia Maria Silva-Veiga, Carolline Santos Miranda, Fabiane Ferreira Martins, Julio Beltrame Daleprane, Carlos Alberto Mandarim-de-Lacerda, and Vanessa Souza-Mello

Oliveira Correia et al. 2019 ), besides mitigating hepatic steatosis in db/db mice ( Michurina et al. 2016 ). Figure 1 illustrates the main sites of actions attributed to the PPAR-alpha agonist and the DPP-4 inhibitor. Figure 1 Main sites of

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Ashley Patton, Tyler Church, Caroline Wilson, Jean Thuma, Douglas J Goetz, Darlene E Berryman, Edward O List, Frank Schwartz, and Kelly D McCall

). Specifically, NAFLD is a disease of excess fat accumulation in the liver of individuals with no history of alcohol abuse, which can range from benign steatosis to advanced steatohepatitis (NASH) and cirrhosis ( El-Serag & Kanwal 2014 ). NASH is associated with

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Paramita M Ghosh, Zhen-Ju Shu, Bing Zhu, Zhongding Lu, Yuji Ikeno, Jeffrey L Barnes, Chih-Ko Yeh, Bin-Xian Zhang, Michael S Katz, and Amrita Kamat

), includes a spectrum of pathological conditions ranging from hepatic steatosis, or augmented fat accumulation in the liver, through steatohepatitis, cirrhosis, and hepatocellular carcinoma ( Clark 2006 , Kotronen et al . 2007 , Stefan et al . 2008

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Caroline E Geisler and Benjamin J Renquist

2 diabetes and metabolic syndrome in recent decades ( Tuyama & Chang 2012 , Yki-Jarvinen 2016 ). NAFLD encompasses hepatic steatosis driven by factors other than excessive alcohol consumption and is estimated to affect 25% of the global population

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Sihan Lv, Xinchen Qiu, Jian Li, Jinye Liang, Weida Li, Chao Zhang, Zhen-Ning Zhang, and Bing Luan

& Karin 2012 ). Disrupted lipid metabolism including fatty acid oxidation and de novo lipogenesis in liver results in the development of hepatic steatosis and contributes to the development of hepatic insulin resistance ( Marchesini et al . 2003

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Giselle Adriana Abruzzese, Maria Florencia Heber, Silvana Rocio Ferreira, Leandro Martin Velez, Roxana Reynoso, Omar Pedro Pignataro, and Alicia Beatriz Motta

clinicopathologic spectrum of conditions that encompass from simple steatosis (triglyceride (TG) accumulation in hepatocytes) to steatohepatitis with inflammation, fibrosis and even cirrhosis ( Browning & Horton 2004 ). NAFLD pathogenesis remains unknown and there

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Jing Zhou, Honggui Li, Yuli Cai, Linqiang Ma, Destiny Matthews, Bangchao Lu, Bilian Zhu, Yanming Chen, Xiaoxian Qian, Xiaoqiu Xiao, Qifu Li, Shaodong Guo, Yuqing Huo, Liang Zhao, Yanan Tian, Qingsheng Li, and Chaodong Wu

Introduction Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive fat deposition in hepatocytes (steatosis) ( Browning et al. 2004 , Sanyal 2005 ). When the liver displays overt inflammatory damage due to fat deposition

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Vitaly Ablamunits, Simon Klebanov, Sharon Y Giese, and Kevan C Herold

% formal saline, paraffin embedded, and stained with hematoxylin and eosin (H&E). Morphology was studied using Axioplan 2 microscope (Carl Zeiss Microimaging, Inc., Thornwood, NY, USA). The degree of hepatic steatosis was evaluated semi-quantitatively by

Open access

Dawn E W Livingstone, Emma M Di Rollo, Tracy C-S Mak, Karen Sooy, Brian R Walker, and Ruth Andrew

αR2) develop obesity and insulin resistance, with increased susceptibility to liver steatosis, fibrosis and hepatocellular carcinoma ( Dowman et al. 2013 , Livingstone et al. 2015 ). These findings translate into humans, where dutasteride (a dual