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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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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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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

Open access

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

Gestational diabetes mellitus increases the risk of dysglycemia postpartum in part due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low-protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of proinflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.

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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

abnormalities. Indeed, genetic deletion of their components, such as NLRP3, caspase 1, ASC and IL1b, improved glucose metabolism in diet-induced obesity ( Stienstra et al. 2010 , 2011 ). However, the pathophysiological relationship between the inflammasome

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

intolerance and insulin signaling. We also show that EPO does not target the skeletal muscle cell indicating an indirect action through the improvement of several systemic factors known to be beneficial for whole-body glucose metabolism. Materials and methods