, Fowden et al . 2006 , Seckl 2008 ). Similarly, in naturally occurring IUGR in polytocous species, low birth weight is associated with adult glucose intolerance and altered fat deposition ( Poore & Fowden 2002 , 2004 ). In both naturally occurring and
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K L Franko, A J Forhead, and A L Fowden
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
Alena Nareika, Yeong-Bin Im, Bryan A Game, Elizabeth H Slate, John J Sanders, Steven D London, Maria F Lopes-Virella, and Yan Huang
& McGee 1979 , Pyorala et al . 1987 , Position paper 1999 ). Dandona et al. have shown in their patient studies that increased glucose concentration following a glucose load leads to an increase in the expression by mononuclear cells of tumor necrosis
Akiko Mizokami, Satoru Mukai, Jing Gao, Tomoyo Kawakubo-Yasukochi, Takahito Otani, Hiroshi Takeuchi, Eijiro Jimi, and Masato Hirata
diabetic condition by affecting multiple aspects of systemic glucose and energy metabolism ( Lee et al. 2007 a , Ferron et al. 2008 , 2010 , Fulzele et al. 2010 ) in a manner dependent on interaction with its putative receptor GPRC6A ( Oury et
Risheng Ye, Min Ni, Miao Wang, Shengzhan Luo, Genyuan Zhu, Robert H Chow, and Amy S Lee
transgenic mouse strains with Grp78 promoter deletions. Fortuitously, we observed progressive glucose intolerance in one of the transgenic mouse lines, referred to below as D2D, as a consequence of the genomic integration site of the transgene. With inverse
Susan Gray, Barbara S Stonestreet, Shanthie Thamotharan, Grazyna B Sadowska, Molly Daood, Jon Watchko, and Sherin U Devaskar
. 1998 ). Corticosteroids have also been shown to have major effects on fetal glucose homeostasis resulting in long-term persistence of these changes after birth in sheep and rats ( Nyirenda et al. 1998 , 2001 , Gatford et al. 2000 , Sloboda et al
Xin-gang Yao, Xin Xu, Gai-hong Wang, Min Lei, Ling-ling Quan, Yan-hua Cheng, Ping Wan, Jin-pei Zhou, Jing Chen, Li-hong Hu, and Xu Shen
normal metabolic demand ( Leahy 1990 ). Pathologically, dysfunction of β-cells is characterized by the loss of glucose-stimulated insulin secretion (GSIS) and β-cell death that leads to a reduction in insulin content and β-cell mass. Thus, amelioration of
Wanying Qin, Ting Zhang, Mingxia Ge, Huimin Zhou, Yuhui Xu, Rongfang Mu, Chaoguang Huang, Daowei Liu, Bangrui Huang, Qian Wang, Qinghua Kong, Qingpeng Kong, Fei Li, and Wenyong Xiong
Introduction Liver is a key governing hub of mammalian body glucose and lipid metabolism, which communicates with the circulatory system with mechanisms depending on the energy status. In the fed state, the liver takes in dietary glucose from
Andreas Börjesson and Carina Carlsson
determined ( Leahy et al. 1991 , Leahy 1993 , Alarcon et al. 1995 , Gadot et al. 1995 ). Biosynthesis of proinsulin in β-cells is stimulated by glucose and this imposes an increased demand on the mechanism for proinsulin to insulin conversion
S Patterson, P R Flatt, L Brennan, P Newsholme, and N H McClenaghan
plasma glucose levels results in glycation of endogenous proteins, sustained secretory hyper-activity, and the eventual loss of glucose sensitivity and β-cell exhaustion ( Malaisse 1991 , 1994 , Ling & Pipeleers 1996 ). Glucose can exert toxic
