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Guillermo Vazquez-Anaya, Bridget Martinez, José G Soñanez-Organis, Daisuke Nakano, Akira Nishiyama and Rudy M Ortiz

, Aguer & Harper 2012 ). Both hyperthyroidism and hypothyroidism have been associated with complications in insulin signaling and glucose intolerance, a paradox that is likely associated with differential effects of TH on various tissues ( Brenta 2010

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Irene Andrés-Blasco, Andrea Herrero-Cervera, Ángela Vinué, Sergio Martínez-Hervás, Laura Piqueras, María Jesús Sanz, Deborah Jane Burks and Herminia González-Navarro

increasing at an alarming rate due to population aging and to sedentary lifestyle patterns ( Wild et al . 2004 ). Metabolic alterations that define MetS include insulin resistance (IR), abdominal obesity, glucose intolerance, hypertension and dyslipidemia

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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

prevent and/or reverse HF diet-induced hepatic and adipose tissue inflammation as well as hepatic steatosis and glucose intolerance in a diet-induced obesity (DIO) mouse model. Materials and methods Phenylmethimazole (C10) solutions

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Min Kyong Moon, In-Kyong Jeong, Tae Jung Oh, Hwa Young Ahn, Hwan Hee Kim, Young Joo Park, Hak Chul Jang and Kyong Soo Park

the neonatal period ( Howdeshell et al . 1999 , Rubin et al . 2001 , Rubin & Soto 2009 ). However, Ryan et al . (2010) reported a contrary result that oral exposure to BPA during the perinatal period did not induce glucose intolerance later in

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Sandra K Szlapinski, Anthony A Botros, Sarah Donegan, Renee T King, Gabrielle Retta, Brenda J Strutt and David J Hill

). Clinical studies have shown that glucose intolerance after parturition involves β-cell dysfunction ( Buchanan & Xiang 2005 , Retnakaran et al. 2008 , Xiang et al. 2010 , Molęda et al. 2013 ) which can occur, in part, due to inflammation and

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Salvatore P Mangiafico, Shueh H Lim, Sandra Neoh, Helene Massinet, Christos N Joannides, Joseph Proietto, Sofianos Andrikopoulos and Barbara C Fam

Introduction Type 2 diabetes (T2D) is characterised by glucose intolerance that is contributed to by both defects in insulin action (in liver and muscle/fat) and insulin secretion. Whether defects in both insulin action and secretion are necessary

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Greg M Kowalski, Michael J Kraakman, Shaun A Mason, Andrew J Murphy and Clinton R Bruce

mouse is one of, if not the most commonly used model of metabolic disease and prediabetes as it rapidly and robustly develops obesity, insulin resistance and glucose intolerance ( Surwit et al . 1988 , 1991 , Winzell & Ahren 2004 , Turner et al

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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

and glucose intolerance ( Härndahl et al. 2004 ). Another mouse line with lower, 2–3-fold over-expression (RIP-PDE3B/2) exhibits less severe features. However, they display reduced glucose-stimulated insulin secretion concomitant with islet

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Tsutomu Wada, Akari Ishikawa, Eri Watanabe, Yuto Nakamura, Yusuke Aruga, Hayate Hasegawa, Yasuhiro Onogi, Hiroe Honda, Yoshinori Nagai, Kiyoshi Takatsu, Yoko Ishii, Masakiyo Sasahara, Daisuke Koya, Hiroshi Tsuneki and Toshiyasu Sasaoka

Obesity-associated activation of the renin-angiotensin-aldosterone system is implicated in the pathogenesis of insulin resistance; however, influences of mineralocorticoid receptor (MR) inhibition remain unclear. Therefore, we aimed to clarify the anti-inflammatory mechanisms of MR inhibition using eplerenone, a selective MR antagonist, in C57BL/6 mice fed a high-fat diet (HFD) for 12 weeks. Eplerenone prevented excessive body weight gain and fat accumulation, ameliorated glucose intolerance and insulin resistance and enhanced energy metabolism. In the epididymal white adipose tissue (eWAT), eplerenone prevented obesity-induced accumulation of F4/80+CD11c+CD206-M1-adipose tissue macrophage (ATM) and reduction of F4/80+CD11cCD206+-M2-ATM. Interestingly, M1-macrophage exhibited lower expression levels of MR, compared with M2-macrophage, in the ATM of eWAT and in vitro-polarized bone marrow-derived macrophages (BMDM). Importantly, eplerenone and MR knockdown attenuated the increase in the expression levels of proIl1b, Il6 and Tnfa, in the eWAT and liver of HFD-fed mice and LPS-stimulated BMDM. Moreover, eplerenone suppressed IL1b secretion from eWAT of HFD-fed mice. To reveal the anti-inflammatory mechanism, we investigated the involvement of NLRP3-inflammasome activation, a key process of IL1b overproduction. Eplerenone suppressed the expression of the inflammasome components, Nlrp3 and Caspase1, in the eWAT and liver. Concerning the second triggering factors, ROS production and ATP- and nigericin-induced IL1b secretion were suppressed by eplerenone in the LPS-primed BMDM. These results indicate that eplerenone inhibited both the priming and triggering signals that promote NLRP3-inflammasome activation. Therefore, we consider MR to be a crucial target to prevent metabolic disorders by suppressing inflammasome-mediated chronic inflammation in the adipose tissue and liver under obese conditions.

Open access

Corinne Caillaud, Mie Mechta, Heidi Ainge, Andreas N Madsen, Patricia Ruell, Emilie Mas, Catherine Bisbal, Jacques Mercier, Stephen Twigg, Trevor A Mori, David Simar and Romain Barrès

significantly lower levels in HFD/EPO compared with HFD; Table 1 ), indicating that EPO may participate in the decrease in systemic inflammation. To determine the role of EPO in oxidative stress in our model of HFD-induced glucose intolerance, we quantified