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Yuumi Ishizuka, Kazuhiro Nakayama, Ayumi Ogawa, Saho Makishima, Supichaya Boonvisut, Atsushi Hirao, Yusaku Iwasaki, Toshihiko Yada, Yoshiko Yanagisawa, Hiroshi Miyashita, Masafumi Takahashi, Sadahiko Iwamoto and Jichi Medical University Promotion Team of a Large-Scale Human Genome Bank for All over Japan

and eosin (H&E), Oil Red O, or PAS. Hepatocyte apoptosis was assessed using a colorimetric TUNEL System (Promega). Mice that had fasted for 12 h were injected with glucose (1.8 g/kg) or insulin (1 U/kg) i.p. for glucose tolerance test (GTT) and insulin

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Andrea Armani, Vincenzo Marzolla, Andrea Fabbri and Massimiliano Caprio

high-fat-diet-induced weight gain, protection from fat mass expansion and impaired glucose tolerance, thus showing beneficial metabolic effects similar to those observed in obese mice treated with MR antagonists ( Hirata et al . 2009 , Wada et al

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Qi Zhang, Qin Zhu, Ruyuan Deng, Feiye Zhou, Linlin Zhang, Shushu Wang, Kecheng Zhu, Xiao Wang, Libin Zhou and Qing Su

2012 ). Treatment of db/db mice with MS-275, a class I-specific HDAC inhibitor, resulted in increased glucose tolerance, insulin sensitivity and clearance of liver lipids, as well as decreased plasma triglycerides and free fatty acids ( Galmozzi et al

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Long The Nguyen, Sonia Saad, Yi Tan, Carol Pollock and Hui Chen

). Intraperitoneal glucose tolerance test (IPGTT) At P19, the animals were weighed and fasted for 5 h prior to IPGTT ( Chen et al . 2009 ), then a glucose solution (50%) was injected (2 g/kg, i.p.). Tail blood glucose level was recorded prior to glucose injection

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Weijuan Shao, Vivian Szeto, Zhuolun Song, Lili Tian, Zhong-Ping Feng, M Cristina Nostro and Tianru Jin

). When the RIP promoter was utilized to drive the expression of the mouse TCF7L2DN, the generated transgenic mouse lines showed impaired glucose tolerance and decreased insulin secretion, associated with a marked reduction of β-cell mass and decreased

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Suzy S J Hur, Jennifer E Cropley and Catherine M Suter

maternal caloric restriction) leads to low birthweight not only in those males but also in their progeny ( Jimenez-Chillaron et al . 2009 ). The progeny also exhibit defective glucose tolerance linked to impaired β-cell function, as well as defects in

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Y Y Liu, W Jia, I E Wanke, D A Muruve, H P Xiao and N C W Wong

complied with guidelines at University of Calgary. Intraperitoneal glucose tolerance test Mice fasted >6 h were injected i.p. with 2 g/kg glucose ( Davalli et al . 1995 ) and glucose monitored 15 or 30 min up to 120 min. Serum assays Serum was separated

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Elena Ivanova and Gavin Kelsey

resistance Germain-Lee et al . (2005) Reduced metabolic rate, energy expenditure and locomotor activity, severe obesity, insulin resistance and impaired glucose tolerance Chen et al . (2005) Brain-specific knockout (maternal transmission) Obesity, reduced

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Rihua Zhang, Dongming Su, Weidong Zhu, Qiong Huang, Menglan Liu, Yi Xue, Yuanyuan Zhang, Dong li, Allan Zhao and Yun Liu

Szklo M Gapstur S Kopp P Liu K Ouyang P 2007 Endogenous sex hormones and glucose tolerance status in postmenopausal women . Journal of Clinical Endocrinology and Metabolism 92 1289 – 1295 . ( doi:10.1210/jc.2006-1895 ). Grabe N

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Yan Zheng and Kevin D Houston

impaired glucose tolerance within 6 months of age ( Martensson et al. 2009 ). Of note, both classical and non-classical estrogen signaling regulates glucose uptake, glucose storage, insulin secretion and has a role in insulin sensitivity ( Brown & Clegg