enhanced or reduced embryonic survival (ES) ( O'Connell et al . 2013 ). Therefore, these animals provide a powerful and unique animal model to identify maternal pathways that are potentially important for survival of the embryo. The activin pathway has
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Anne R O'Connell, Kenneth P McNatty, Peter R Hurst, Thomas E Spencer, Fuller W Bazer, Karen L Reader, Peter D Johnstone, George H Davis, and Jennifer L Juengel
T Clark Brelje, Nicholas V Bhagroo, Laurence E Stout, and Robert L Sorenson
secretion shown in Fig. 1 B). These results demonstrate that prior culture with palmitate can actually enhance the effects of prolactin on insulin secretion when stimulated with glucose in the presence of palmitate. As this is the likely condition in vivo
Jiean Xu, Qiuhua Yang, Xiaoyu Zhang, Zhiping Liu, Yapeng Cao, Lina Wang, Yaqi Zhou, Xianqiu Zeng, Qian Ma, Yiming Xu, Yong Wang, Lei Huang, Zhen Han, Tao Wang, David Stepp, Zsolt Bagi, Chaodong Wu, Mei Hong, and Yuqing Huo
that endothelial-specific Adk deficiency had a glucose-lowering effect on mice fed a chow diet (CD) and protected mice from high-fat-diet (HFD)-induced insulin resistance and metabolic syndrome, which was associated with an enhancement of NO
Zhenhua Li, Tao Zhang, Hongyan Dai, Guanghui Liu, Haibin Wang, Yingying Sun, Yun Zhang, and Zhiming Ge
. 2006 ). One major pathway of UPR is to increase regulation of the expression of ER-localized molecular chaperons, such as glucose-regulated protein 78 (GRP78), which can contribute to repairing unfolded proteins. The early UPR enhances cell survival by
XingJia Wang, Chwan-Li Shen, Matthew T Dyson, Xianling Yin, Randolph B Schiffer, Paula Grammas, and Douglas M Stocco
cells increased the synthesis of 5-lipoxygenase-generated metabolites of AA, namely, 5-hydroperoxyeicosatetraenoic acid (5-HPETE) and 5-hydroxyeicosatetraenoic acid (5-HETE), both of which enhanced cAMP-stimulated StAR expression ( Wang et al. 2003 b
Y-H Suh, S-Y Kim, H-Y Lee, B C Jang, J H Bae, J-N Sohn, J-H Bae, S-I Suh, J-W Park, K-U Lee, and D-K Song
SHP enhanced GSIS in normal and UCP2-overexpressing β-cells, probably not via PPARγ activation but through potentiating glucose metabolism in the mitochondria. Materials and Methods Materials Fura-2
Hidetada Ogata, Yusuke Seino, Norio Harada, Atsushi Iida, Kazuyo Suzuki, Takako Izumoto, Kota Ishikawa, Eita Uenishi, Nobuaki Ozaki, Yoshitaka Hayashi, Takashi Miki, Nobuya Inagaki, Shin Tsunekawa, Yoji Hamada, Susumu Seino, and Yutaka Oiso
of pancreatic islets ( Miki et al . 1998 ). In contrast to GIIS, GIP secretion in response to oral glucose loading in Kir6.2 −/− mice is somewhat enhanced, compared with that in Kir6.2 + / + mice ( Miki et al . 2005 ). This indicates that the K
T Sakurai, K Tamura, and H Kogo
luteal cells treated with 0.3–10 ng/ml VEGF showed a dose-dependent increase in their production of COX-II mRNA. In contrast, COX-I mRNA levels did not change. When we assessed the kinetics of the VEGF-induced enhancement of COX-II mRNA levels, we found
Muneaki Ishijima, Kunikazu Tsuji, Susan R Rittling, Teruhito Yamashita, Hisashi Kurosawa, David T Denhardt, Akira Nifuji, Yoichi Ezura, and Masaki Noda
reported that OPN is necessary for unloading-induced enhancement of bone resorption and suppression of bone formation in vivo ( Ishijima et al. 2001 , 2002 ). These data suggest that OPN plays a key role in conveying the effect of mechanical stress
V L Clifton, R Crompton, M A Read, P G Gibson, R Smith, and I M R Wright
described reduced peripheral vasoconstriction during the follicular phase ( Freedman & Girgis 2000 , Chan et al. 2001 ) and enhanced endothelial-dependent vasodilation in the presence of increased estrogen concentrations during the menstrual cycle
