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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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André Sarmento-Cabral, Mercedes del Rio-Moreno, Mari C. Vazquez-Borrego, Mairyah Mahmood, Elena Guiterrez-Casado, Natalie Pelke, Grace Guzman, Papasani V Subbaiah, Jose Cordoba-Chacon, Shoshana Yakar, and Rhonda D Kineman

A reduction in hepatocyte growth hormone (GH)-signaling promotes non-alcoholic fatty liver disease (NAFLD). However, debate remains as to the relative contribution of the direct effects of GH on hepatocyte function versus indirect effects, via alterations in insulin-like growth factor 1 (IGF1). To isolate the role of hepatocyte GH receptor (GHR) signaling, independent of changes in IGF1, mice with adult-onset, hepatocyte-specific GHR knockdown (aHepGHRkd) were treated with a vector expressing rat IGF1 targeted specifically to hepatocytes. Compared to GHR-intact mice, aHepGHRkd reduced circulating IGF1 and elevated GH. In male aHepGHRkd, the shift in IGF1/GH did not alter plasma glucose or non-esterified fatty acids (NEFA), but was associated with increased insulin, enhanced systemic lipid oxidation and reduced white adipose tissue (WAT) mass. Livers of male aHepGHRkd exhibited steatosis associated with increased de novo lipogenesis, hepatocyte ballooning and inflammation. In female aHepGHRkd, hepatic GHR protein levels were not detectable, but moderate levels of IGF1 were maintained, with minimal alterations in systemic metabolism and no evidence of steatosis. Reconstitution of hepatocyte IGF1 in male aHepGHRkd lowered GH and normalized insulin, whole body lipid utilization and WAT mass. However, IGF1 reconstitution did not reduce steatosis or eliminate liver injury. RNAseq analysis showed IGF1 reconstitution did not impact aHepGHRkd-induced changes in liver gene expression, despite changes in systemic metabolism. These results demonstrate the impact of aHepGHRkd is sexually dimorphic and the steatosis and liver injury observed in male aHepGHRkd mice is autonomous of IGF1, suggesting GH acts directly on the adult hepatocyte to control NAFLD progression.

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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