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Kok Lim Kua, Shanming Hu, Chunlin Wang, Jianrong Yao, Diana Dang, Alexander B Sawatzke, Jeffrey L Segar, Kai Wang and Andrew W Norris

insulin resistance by hyperglycemia is not entirely surprising, as in vivo ( Oku et al. 2001 , Haber et al. 2003 ) and in vitro ( Kurowski et al. 1999 ) experiments demonstrate that hyperglycemia acutely induces insulin resistance in mature

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Li Li, Xiaohua Li, Wenjun Zhou and Joseph L Messina

studies have included models of chronic psychological stress, with few studies on the effects of acute psychological stress on metabolic dysfunction and insulin resistance ( Depke et al . 2008 , Tamashiro et al . 2011 , Finger et al . 2012 ). We

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Lidong Zhai and Joseph L Messina

Introduction Acute insulin resistance is common following trauma, hemorrhage, sepsis, burn, and critical illness ( Ikezu et al . 1997 , Carter 1998 , Van den Berghe et al . 2001 , Cree & Wolfe 2008 ). Chronic insulin resistant states, such as

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Mathias Fasshauer, Johannes Klein, Susan Kralisch, Margit Klier, Ulrike Lossner, Matthias Bluher and Ralf Paschke

. Furthermore, the authors demonstrated that SAA3 is stimulated by TNFα which has been shown to induce insulin resistance in vivo and in vitro ( Lin et al. 2001 ). Thus, the data accumulated so far suggest that SAA3 is not only a well-known acute

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Edward Park, Victor Wong, Xinyu Guan, Andrei I Oprescu and Adria Giacca

mechanism than short-term FFA elevation. Thus, in the present study, we wished to test the hypothesis that IKKβ activation is causally involved in the mechanism of hepatic insulin resistance induced by acute FFA elevation. To do this, we used a rat model of

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Anna G Holmes, Jose L Mesa, Bronwyn A Neill, Jason Chung, Andrew L Carey, Gregory R Steinberg, Bruce E Kemp, Robert J Southgate, Graeme I Lancaster, Clinton R Bruce, Matthew J Watt and Mark A Febbraio

insulin resistance ( Ueki et al . 2004 ), while acute doses of IL-6 may not result in a sustained increase in SOCS3 necessary to disrupt insulin signalling. Accordingly, in the present study we tested the hypothesis that chronic elevation of IL-6 may

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Aoife Kiely, Aisling Robinson, Neville H McClenaghan, Peter R Flatt and Philip Newsholme

innate immune product receptors, e.g. TLRs, in insulin resistance has been recently published ( Tsukumo et al . 2007 ). Notably type 2 diabetes has been associated with chronic low-grade inflammation ( Creely et al . 2007 ) in addition to the well

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David P Macfarlane, Shareen Forbes and Brian R Walker

manifestations of Cushing's syndrome are predictable on the basis of the acute effects of glucocorticoids (e.g. to raise blood pressure, induce insulin resistance, promote skeletal muscle wasting and elevate plasma glucose), it appears to be a paradox that the

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Rita Sharma, Quyen Luong, Vishva M Sharma, Mitchell Harberson, Brian Harper, Andrew Colborn, Darlene E Berryman, Niels Jessen, Jens Otto Lunde Jørgensen, John J Kopchick, Vishwajeet Puri and Kevin Y Lee

insulin resistance caused by acute GH treatment is reversed by a pharmacological blockade of lipolysis ( Segerlantz et al. 2003 , Moller et al. 2009 , Salgin et al. 2009 , Cornford et al. 2012 ). Additionally, the ‘dawn phenomenon’, which

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Ruben Rodriguez, Jacqueline N Minas, Jose Pablo Vazquez-Medina, Daisuke Nakano, David G Parkes, Akira Nishiyama and Rudy M Ortiz

this study was to determine whether acute and chronic AT 1 blockade started after the onset of obesity, hyperglycemia and hypertension would have beneficial effects on pancreatic function and peripheral insulin resistance. To this end, the present