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Yuriko Sakai, Hideyuki Arie, Yinhua Ni, Fen Zhuge, Liang Xu, Guanliang Chen, Naoto Nagata, Takuya Suzuki, Shuichi Kaneko, Tsuguhito Ota, and Mayumi Nagashimada

). The pathophysiological mechanisms underlying steatosis–NASH progression remain poorly understood. According to the ‘multiple parallel-hit’ theory of NAFLD, oxidative stress, autophagy dysregulation, and aberrant immune and hepatic stellate cell (HSC

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Maria Namwanje, Longhua Liu, Michelle Chan, Nikki Aaron, Michael J Kraakman, and Li Qiang

mass and adipocyte size. In addition, the double-knockout mice, Cbp/p300-AKO , exhibited severe lipodystrophy accompanied by hyperglycemia, hyperlipidemia and hepatic steatosis. Furthermore, we demonstrated that selective inhibition of Cbp and p300

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Gustavo W Fernandes, Cintia B Ueta, Tatiane L Fonseca, Cecilia H A Gouveia, Carmen L Lancellotti, Patrícia C Brum, Marcelo A Christoffolete, Antonio C Bianco, and Miriam O Ribeiro

animals per group. Liver steatosis in ARβ 2 KO mice Feeding on a HFD caused liver steatosis indistinctly in both groups of animals, i.e. ARβ 2 KO and WT animals ( Fig. 4 ). Figure 4 Liver steatosis in ARβ 2 KO mice fed HFD. Liver sections stained by H

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Helena A Walz, Linda Härndahl, Nils Wierup, Emilia Zmuda-Trzebiatowska, Fredrik Svennelid, Vincent C Manganiello, Thorkil Ploug, Frank Sundler, Eva Degerman, Bo Ahrén, and Lena Stenson Holst

in adipocytes from mice on the HFD as compared with adipocytes from CD-fed mice (Fig. 5B P , < 0.05, n =3). Steatosis of the liver is associated with hepatic insulin resistance ( Seppala-Lindroos et al. 2002 ). We therefore decided to

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Adrián Báez-Ruiz, Natalí N Guerrero-Vargas, Fernando Cázarez-Márquez, Elizabeth Sabath, María del Carmen Basualdo, Roberto Salgado-Delgado, Carolina Escobar, and Ruud M Buijs

steatosis (HS), dyslipidemia, disruption of bile acid homeostasis, insulin insensitivity and increased adipose mass ( Ma et al. 2009 , Shimba et al. 2011 , Coomans et al. 2013 , Aoki et al. 2014 ). Interestingly, similar health problems are

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T Mracek, D Gao, T Tzanavari, Y Bao, X Xiao, C Stocker, P Trayhurn, and C Bing

epididymal (C and D) fat. Data are means± s.e.m. for groups of 6. * P <0.05, *** P <0.001 compared with lean controls. ZAG gene and protein expression in liver of ob/ob mice Liver histology revealed the typical features of steatosis (fatty liver) in ob

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W Yin, D Liao, M Kusunoki, S Xi, K Tsutsumi, Z Wang, X Lian, T Koike, J Fan, Y Yang, and C Tang

The synthetic compound NO-1886 (ibrolipim) is a lipoprotein lipase activator that has been proven to be highly effective in lowering plasma triglycerides. Recently, we found that NO-1886 also reduced plasma free fatty acids and glucose in high-fat/high-sucrose diet-induced diabetic rabbits. In the current study, we investigated the effects of NO-1886 treatment on ectopic lipid deposition and the islet pathology in miniature swine fed a high-fat/high-sucrose diet. Our results showed that feeding this diet to miniature swine caused insulin resistance, increased lipid deposition in non-adipose tissue, such as in the heart, skeletal muscle, liver and pancreas, and also caused pancreatic beta cell damage. However, supplementing 1% NO-1886 (200 mg/kg per day) into the high-fat/high-sucrose diet decreased ectopic lipid deposition, improved insulin resistance, and alleviated the beta cell damage. These results suggest that improvement of lipid disorder, non-adipose tissue steatosis and insulin resistance may be very important for the protection of beta cell damage. Therefore, NO-1886 is potentially beneficial for the treatment of insulin-resistance syndrome.

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Mohamed Asrih and François R Jornayvaz

. 2010 , Younossi et al . 2011 ). It is histologically characterized by hepatic triglyceride (TG) accumulation of more than 5%, resulting in steatosis and hepatic inflammation ( Tarantino et al . 2010 ). NAFLD includes a complex spectrum of disorders

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Sarah Teillon, German A Calderon, and Maribel Rios

2003 ). The liver is highly susceptible to chronic increases in dietary fat intake, which elicits hepatic steatosis, reduced hepatic insulin sensitivity, and a concomitant failure to suppress liver glucose output. These deficits are thought to result in

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Maayan Vatarescu, Sapir Bechor, Yulia Haim, Tal Pecht, Tanya Tarnovscki, Noa Slutsky, Ori Nov, Hagit Shapiro, Avishai Shemesh, Angel Porgador, Nava Bashan, and Assaf Rudich

, resulted in decreased hepatic steatosis, insulin resistance and glucose overproduction ( Sabio et al . 2008 , Wueest et al . 2010 , Zhang et al . 2011 ). Compared to this wealth of studies implicating adipose tissue inflammation in the pathogenesis