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

Intestinal mucosal barrier dysfunction is closely related to the pathogenesis of nonalcoholic steatohepatitis (NASH). Gut immunity has been recently demonstrated to regulate gut barrier function. The Lactobacillus pentosus strain S-PT84 activates helper T cells and natural killer/natural killer T cells. In this study, we examined the effect of S-PT84 on NASH progression induced by high-cholesterol/high-fat diet (CL), focusing on the immune responses involved in gut barrier function. C57BL/6 mice were fed a normal chow or CL diet with or without 1 × 1010 S-PT84 for 22 weeks. S-PT84 administration improved hepatic steatosis by decreasing triglyceride and free fatty acid levels by 34% and 37%, respectively. Furthermore, S-PT84 inhibited the development of hepatic inflammation and fibrosis, suppressed F4/80+ macrophage/Kupffer cell infiltration, and reduced liver hydroxyproline content. Administration of S-PT84 alleviated hyperinsulinemia and enhanced hepatic insulin signalling. Compared with mice fed CL diet, mice fed CL+S-PT84 had 71% more CD11c-CD206+ M2 macrophages, resulting in a significantly decreased M1/M2 macrophage ratio in the liver. Moreover, S-PT84 inhibited the CL diet-mediated increase in intestinal permeability. Additionally, S-PT84 reduced the recruitment of interleukin-17-producing T cells and increased the levels of intestinal tight junction proteins, including zonula occludens-1, occludin, claudin-3, and claudin-7. In conclusion, our findings suggest that S-PT84 attenuates diet-induced insulin resistance and subsequent NASH development by maintaining gut permeability. Thus, S-PT84 represents a feasible approach to prevent the development of NASH.

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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

Open access

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

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Rodrigo Martins Pereira, Kellen Cristina da Cruz Rodrigues, Chadi Pellegrini Anaruma, Marcella Ramos Sant’Ana, Thaís Dantis Pereira de Campos, Rodrigo Stellzer Gaspar, Raphael dos Santos Canciglieri, Diego Gomes de Melo, Rania A Mekary, Adelino Sanchez Ramos da Silva, Dennys Esper Cintra, Eduardo Rochete Ropelle, José Rodrigo Pauli, and Leandro Pereira de Moura

Introduction Nonalcoholic fatty liver disease (NAFLD) is a pre-condition for most common liver diseases, and it can be developed from hepatic steatosis, non-alcoholic steatohepatitis (NASH), cirrhosis, to hepatocellular carcinoma (HCC) ( Tilg