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Tusty-Jiuan Hsieh, Pierre Fustier, Chih-Chang Wei, Shao-Ling Zhang, Janos G Filep, Shiow-Shiu Tang, Julie R Ingelfinger, I George Fantus, Pavel Hamet and John S D Chan

expression of angiotensinogen protein and mRNA or activate p44/42 MAPK phosphorylation in diabetic rat RPTCs ( Zhang et al. 2002 a ), suggesting that the effect of hyperglycaemia-induced insulin resistance on the inhibition of ANG gene expression is

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B Maiztegui, M I Borelli, M L Massa, H Del Zotto and J J Gagliardino

Introduction Insulin resistance is a common feature of several pathological conditions characterized by a decreased response of insulin-dependent tissues to the hormone action that triggers a reactive hyperinsulinemia to keep blood

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R H Straub, L B Tankó, C Christiansen, P J Larsen and D S Jessop

Introduction The insulin resistance syndrome is an established risk factor for macrovascular disease and type 2 diabetes, two important health problems among the elderly (more than 65 years; Raji & Plutzky 2002 , Grant & Meigs 2004 ). The presence

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Alex Rafacho, Henrik Ortsäter, Angel Nadal and Ivan Quesada

effects, including peripheral insulin resistance (IR) and glucose intolerance as well as overt hyperglycaemia and diabetes. These side effects are observed particularly in susceptible individuals such as pregnant women, obese subjects, IR individuals or

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Raquel Barbuio, Marciane Milanski, Manoel B Bertolo, Mário J Saad and Lício A Velloso

( Day & James 1998 , Browning & Horton 2004 ). In recent years, the characterization of the frequent association between NASH and hepatic insulin resistance has opened a new venue for investigation in this field ( Medina et al. 2004 ). In

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Haiming Cao

serum fatty acid levels. This overflow of lipids from obese adipose depots has been considered a key reason for obesity-associated insulin resistance and hepatosteatosis for several decades ( Randle et al . 1963 , Samuel et al . 2010 ). But fatty

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Christine M A Martin, Vadivel Parthsarathy, Varun Pathak, Victor A Gault, Peter R Flatt and Nigel Irwin

overnight at 37 °C. Acute tests for insulin release were preceded by 40 min preincubation at 37 °C in 1.0 ml Krebs–Ringer bicarbonate buffer (115 mM NaCl, 4.7 mM KCl, 1.28 mM NaCl 2 , 1.2 mM KH 2 PO 4 , 1.2 mM MgSO 4 , 10 mM NaHCO 3 , 0.5% (w/v) BSA, pH 7

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Weiwei Xu, Jamie Morford and Franck Mauvais-Jarvis

-prandial insulin secretion ( O’Meara et al . 1993 ) or exaggerated acute insulin response to glucose ( Dunaif & Finegood 1996 ). These alterations in β cell function are not explained by insulin resistance. Rather, they are closely associated with testosterone

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Wanpitak Pongkan, Hiranya Pintana, Sivaporn Sivasinprasasn, Thidarat Jaiwongkam, Siriporn C Chattipakorn and Nipon Chattipakorn

testosterone deficiency increases substantially with age ( Araujo et al. 2007 ) and is associated with the development of several disorders including obesity, dyslipidemia, insulin resistance, metabolic syndrome, and cardiovascular disease ( Grossmann et al

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Alison V Roland, Craig S Nunemaker, Susanna R Keller and Suzanne M Moenter

.0001%). All steroids were used at a final concentration of 10 nM. The following day, islets from each steroid treatment group were incubated in standard KRB solution with steroids omitted to preclude acute effects. Insulin release in 3 and 11 mM glucose was