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James E P Brown, David J Onyango, Manjunath Ramanjaneya, Alex C Conner, Snehal T Patel, Simon J Dunmore and Harpal S Randeva

normal, impaired glucose tolerance, and type 2 diabetic subjects . Experimental and Clinical Endocrinology and Diabetes 114 544 – 548 . Lopez-Bermejo A Chico-Julia B Fernandez-Balsells M Recasens M Esteve E Casamitjana R Ricart W

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Yousheng Xu, Yongshun Wang, Jingjin Liu, Wei Cao, Lili Li, Hongwei Du, Enbo Zhan, Ruoxi Zhang, Huimin Liu, Maoen Xu, Tao Chen, Yilin Qu and Bo Yu

systemic insulin sensitivity, glucose tolerance and serum lipid profiles ( Janssen et al. 2002 ). Visceral adipose tissue mass is more closely correlated with obesity-associated metabolic syndromes ( DiPietro et al. 1999 ). The elevated fat mass in

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Sachie Nakamichi, Yoko Senga, Hiroshi Inoue, Aki Emi, Yasushi Matsuki, Eijiro Watanabe, Ryuji Hiramatsu, Wataru Ogawa and Masato Kasuga

injection unless indicated otherwise. For a glucose tolerance test (GTT), mice deprived of food for 16 h were loaded intraperitoneally with glucose (2 g/kg). Blood glucose and plasma insulin concentrations were measured as described ( Miyake et al . 2002

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Chunmei Wang and Yong Xu

-3022(02)00003-1 ) Martensson UE Salehi SA Windahl S Gomez MF Sward K Daszkiewicz-Nilsson J Wendt A Andersson N Hellstrand P Grande PO , 2009 Deletion of the G protein-coupled receptor 30 impairs glucose tolerance, reduces bone growth, increases blood pressure, and

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R Buettner, K G Parhofer, M Woenckhaus, C E Wrede, L A Kunz-Schughart, J Schölmerich and L C Bollheimer

progression from normal glucose tolerance to insulin resistance and overt diabetes mellitus. It can be speculated that in vivo systemic insulinotropic factors (e.g. free fatty acids) may overcome the impairment of pancreatic insulin secretion in order to

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Xinwang Chen, Xiao Jia, Jie Qiao, Youfei Guan and Jihong Kang

al . 2007 ). This discrepancy is difficult to explain. It may result from the different BMI value after weight loss, the type of surgical procedure, or other complex factors such as genetic variation and individual glucose tolerance state. It has

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L A Bach

, constitutive Igfbp2 overexpression reduced postnatal body weight gain in transgenic mice ( Hoeflich et al . 1999 ). Constitutive overexpression also impaired glucose tolerance and decreased GLUT4 glucose transporter translocation to the cell membrane via its

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Inna Astapova

) Src2 −/− (Ncoa2) Lean, increased glucose tolerance, and insulin resistance on high-fat diet. Increased basal and stimulated lipolysis, elevated EE PPARG Picard et al. (2002) Unlikely: the phenotype is opposite of what would be expected in

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Louise Ruby Høj Illum, Stine Thorhauge Bak, Sten Lund and Anders Lade Nielsen

paternal over-nutrition (with the resulting impaired glucose tolerance and increased body weight) to increase the risk of metabolic disease in offspring is well documented. In a study by Ng and coworkers, three-week-old male rats (F0) were fed a HFD for ten

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Yang Mi, Na Guo, Tongqiang He, Jing Ji, Zhibin Li and Pu Huang

/KsJ-Lep db/+ (abbreviated as db/+ ) mouse serves as a promising heterozygous mutant animal model closely mimicking human GDM symptoms ( Kaufmann et al . 1981 ). Prior to pregnancy, they exhibited largely normal glucose tolerance until late gestation