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L Lundholm, G Bryzgalova, H Gao, N Portwood, S Fält, K D Berndt, A Dicker, D Galuska, J R Zierath, J-Å Gustafsson, S Efendic, K Dahlman-Wright and A Khan

in the above reports, after normalizing E 2 dose for body weight. The effects that we observe on glucose tolerance and insulin sensitivity following E 2 treatment are mediated via ERα , since PPT has effects similar to E 2 on glucose metabolism

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Rengasamy Palanivel, Vivian Vu, Min Park, Xiangping Fang and Gary Sweeney

phosphorylation of AMPK (Thr172) and Akt (Thr308 or Ser473). Representative immunoblots together with quantitative analyses (mean± s.e.m. ; n =4) are shown in all cases. We then examined various potential routes of glucose metabolism within the cardiomyocyte

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Eun-Kyung Choi, Woon-Ki Kim, Ok-Joo Sul, Yun-Kyung Park, Eun-Sook Kim, Jae-Hee Suh, Rina Yu and Hye-Seon Choi

. 2012 ). Taken together, we showed that engagement of TNFRSF14 upregulated CD11c expression in BMM via ROS generation, resulting in chronic inflammation which contributes to impaired glucose metabolism due to loss of ovarian function. Understanding the

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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

glucose metabolism in the mitochondria. UCP2 expression is often inversely correlated with the level of reactive oxygen species (ROS) ( Skulachev 1998 ). Although high UCP2 expression can alleviate the cellular load of ROS during energy metabolism ( Echtay

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Louis Potier, Ludovic Waeckel, Fréderic Fumeron, Sophie Bodin, Marinos Fysekidis, Catherine Chollet, Naima Bellili, Fabrice Bonnet, Gaëlle Gusto, Gilberto Velho, Michel Marre, François Alhenc-Gelas, Ronan Roussel, Nadine Bouby and the DESIR study group

beneficial effect on glucose metabolism of ACE inhibition and AT1 receptor blockade observed in clinical trials. This hypothesis is further supported by experimental studies documenting improvement mediated by kinins of insulin resistance during ACE inhibitor

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Darryl L Hadsell, Walter Olea, Nicole Lawrence, Jessy George, Daniel Torres, Takahashi Kadowaki and Adrian V Lee

, increases also occur in the expression and/or activation of enzymes associated with glucose metabolism such as hexokinase II, Glut 1, Glut 12, and PFK2 ( Sochor et al. 1984 , Kaselonis et al. 1999 , Nemeth et al. 2000 , Macheda et al. 2003

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T Mokuno, K Uchimura, R Hayashi, N Hayakawa, M Makino, M Nagata, H Kakizawa, Y Sawai, M Kotake, N Oda, A Nakai, A Nagasaka and M Itoh

The deterioration of glucose metabolism frequently observed in hyperthyroidism may be due in part to increased gluconeogenesis in the liver and glucose efflux through hepatocyte plasma membranes. Glucose transporter 2 (GLUT 2), a facilitative glucose transporter localized to the liver and pancreas, may play a role in this distorted glucose metabolism. We examined changes in the levels of GLUT 2 in livers from rats with l-thyroxine-induced hyperthyroidism or methimazole-induced hypothyroidism by using Western blotting to detect GLUT 2. An oral glucose tolerance test revealed an oxyhyperglycemic curve (impaired glucose tolerance) in hyperthyroid rats (n=7) and a flattened curve in hypothyroid rats (n=7). GLUT 2 levels in hepatocyte plasma membranes were significantly increased in hyperthyroid rats and were not decreased in hypothyroid rats compared with euthyroid rats. The same results were obtained with a densitometric assay. These findings suggest that changes in the liver GLUT 2 concentration may contribute to abnormal glucose metabolism in thyroid disorders.

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Hu Huang, Kaoruko Tada Iida, Hirohito Sone, Tomotaka Yokoo, Nobuhiro Yamada and Ryuichi Ajisaka

effect of adiponectin on glucose homeostasis in individual organs might be, at least in part, regulated at the expression level of the adiponectin receptor. Skeletal muscle and liver are major organs involved in glucose metabolism. In addition

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Nikolaos Nikolaou, Anastasia Arvaniti, Nathan Appanna, Anna Sharp, Beverly A Hughes, Dena Digweed, Martin J Whitaker, Richard Ross, Wiebke Arlt, Trevor M Penning, Karen Morris, Sherly George, Brian G Keevil, Leanne Hodson, Laura L Gathercole and Jeremy W Tomlinson

decreased following dexamethasone treatment, indicative of decreased AKR1D1 activity (C). Data are presented as mean ±  s.e. of n  = 14 participants, *** P  < 0.001. AKR1D1 knockdown alters glucose metabolism gene expression through FXR, GR

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Camilla Alexanderson, Elias Eriksson, Elisabet Stener-Victorin, Malin Lönn and Agneta Holmäng

, the mechanisms for the effects of early exposure to sex steroids on glucose metabolism in adulthood have not been studied as yet. Skeletal muscle handles 75% of all insulin-mediated glucose disposal and is the most important tissue in insulin