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Antonella Amato, Sara Baldassano and Flavia Mulè

liver expresses GLP2R ( El-Jamal et al . 2014 ); however, nothing is known about other species, including humans. Moreover, fatty liver is strongly associated with insulin resistance ( Asrih & Jornayvaz 2013 ), and non-alcoholic hepatic steatosis has

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Chaoyi Zhang, Qianli Zhang, Zhihong Huang and Quan Jiang

). Adropin-knockout mice exhibit increased adiposity, fasting triglycerides and hepatic steatosis ( Ganesh Kumar et al. 2012 ). Moreover, intraperitoneal administration of adropin to hyperlipidemic rats for 10 days was extremely effective in decreasing the

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João Paulo G Camporez, Mohamed Asrih, Dongyan Zhang, Mario Kahn, Varman T Samuel, Michael J Jurczak and François R Jornayvaz

biomarker of NAFLD ( Dushay et al . 2010 , Morris-Stiff & Feldstein 2010 ). In diet-induced obese mice, which have already increased levels of FGF21, suggesting a state of FGF21 resistance, chronic administration of FGF21 reverses hepatic steatosis and

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Bel M Galmés-Pascual, Antonia Nadal-Casellas, Marco Bauza-Thorbrügge, Miquel Sbert-Roig, Francisco J García-Palmer, Ana M Proenza, Magdalena Gianotti and Isabel Lladó

role on the protection of liver from steatosis has been associated with a combined and balanced effect on lipid synthesis and secretion, and on mitochondrial biogenesis and function ( Sonoda et al. 2007 , Chambers et al. 2012 , Bellafante et al

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Akiko Mizokami, Satoru Mukai, Jing Gao, Tomoyo Kawakubo-Yasukochi, Takahito Otani, Hiroshi Takeuchi, Eijiro Jimi and Masato Hirata

intraperitoneal injection of GluOC, a more practical mode of administration, was as effective as was delivery with the osmotic pump. In addition to improving glucose handling, intermittent GluOC injections reversed hepatic steatosis induced by a high-fat diet and

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Jillian L Rourke, Shanmugam Muruganandan, Helen J Dranse, Nichole M McMullen and Christopher J Sinal

under the curve (AUC) for insulin was calculated using the Prism6 Software (La Jolla, CA, USA). Liver steatosis, adipocyte hypertrophy, and inflammation are common features of obesity, contributing to the development of glucose intolerance. Gpr1 WT

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Rachel Botchlett, Shih-Lung Woo, Mengyang Liu, Ya Pei, Xin Guo, Honggui Li and Chaodong Wu

various tissues causing steatosis and systemic insulin resistance. For example, increased FFAs impair the insulin signal in muscle ( Kim et al. 2002 ) and markedly stimulate hepatic gluconeogenesis ( Chu et al. 2002 ), which contribute to increased

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Zhe-Zhen Liao, Xiao-Yan Qi, Ya-Di Wang, Jiao-Yang Li, Qian-Qian Gu, Can Hu, Yin Hu, Heng Sun, Li Ran, Jing Yang, Jiang-Hua Liu and Xin-Hua Xiao

) Mottillo EP Desjardins EM Crane JD Smith BK Green AE Ducommun S Henriksen TI Rebalka IA Razi A Sakamoto K , et al . 2016 Lack of adipocyte AMPK exacerbates insulin resistance and hepatic steatosis through brown and beige adipose

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Richard R Almon, Debra C DuBois, William Lai, Bai Xue, Jing Nie and William J Jusko

of excessive glycogen deposition in the liver associated with human diabetes ( Vallance-Owen 1952 , Clore et al . 1992 ). Much more common is the excessive buildup of fat in the liver (steatosis; Lonardo et al . 2005 ). In the present study, we

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Carsten T Herz and Florian W Kiefer

. 2018 ). Whereas decreasing hypothalamic AMPK activity seems to confer some metabolic benefits, the loss of adipocyte AMPK exacerbates insulin resistance and hepatic steatosis through impaired brown and beige fat function ( Mottillo et al. 2016