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Sabina Paglialunga, Patrick Schrauwen, Christian Roy, Esther Moonen-Kornips, Huiling Lu, Matthijs K C Hesselink, Yves Deshaies, Denis Richard and Katherine Cianflone

) with no change in skeletal muscle GLUT-4 protein levels as assessed by western analysis (data not shown). Evaluation of fatty acid oxidation The increased food intake despite similar weight gain in C5L2KO-LF mice

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MC Sugden, HS Lall, RA Harris and MJ Holness

The pyruvate dehydrogenase kinases (PDK1-4) regulate glucose oxidation through inhibitory phosphorylation of the pyruvate dehydrogenase complex (PDC). Immunoblot analysis with antibodies raised against recombinant PDK isoforms demonstrated changes in PDK isoform expression in response to experimental hyperthyroidism (100 microg/100 g body weight; 3 days) that was selective for fast-twitch vs slow-twitch skeletal muscle in that PDK2 expression was increased in the fast-twitch skeletal muscle (the anterior tibialis) (by 1. 6-fold; P<0.05) but not in the slow-twitch muscle (the soleus). PDK4 protein expression was increased by experimental hyperthyroidism in both muscle types, there being a greater response in the anterior tibialis (4.2-fold increase; P<0.05) than in the soleus (3.2-fold increase; P<0.05). The hyperthyroidism-associated up-regulation of PDK4 expression was observed in conjunction with suppression of skeletal-muscle PDC activity, but not suppression of glucose uptake/phosphorylation, as measured in vivo in conscious unrestrained rats (using the 2-[(3)H]deoxyglucose technique). We propose that increased PDK isoform expression contributes to the pathology of hyperthyroidism and to PDC inactivation by facilitating the operation of the glucose --> lactate --> glucose (Cori) and glucose --> alanine --> glucose cycles. We also propose that enhanced relative expression of the pyruvate-insensitive PDK isoform (PDK4) in skeletal muscle in hyperthyroidism uncouples glycolytic flux from pyruvate oxidation, sparing pyruvate for non-oxidative entry into the tricarboxylic acid (TCA) cycle, and thereby supporting entry of acetyl-CoA (derived from fatty acid oxidation) into the TCA cycle.

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Sihan Lv, Xinchen Qiu, Jian Li, Jinye Liang, Weida Li, Chao Zhang, Zhen-Ning Zhang and Bing Luan

& Karin 2012 ). Disrupted lipid metabolism including fatty acid oxidation and de novo lipogenesis in liver results in the development of hepatic steatosis and contributes to the development of hepatic insulin resistance ( Marchesini et al . 2003

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Eun Hee Koh, Ah-Ram Kim, Hyunshik Kim, Jin Hee Kim, Hye-Sun Park, Myoung Seok Ko, Mi-Ok Kim, Hyuk-Joong Kim, Bum Joong Kim, Hyun Ju Yoo, Su Jung Kim, Jin Sun Oh, Chang-Yun Woo, Jung Eun Jang, Jaechan Leem, Myung Hwan Cho and Ki-Up Lee

, proton leakage, maximal OCR, reserve capacity and non-mitochondrial OCR) were analyzed as described by Hill et al . (2012) ( Supplementary Figure 2 , see section on supplementary data given at the end of this article). Fatty acid oxidation The fatty

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Sung-Soo Park, Yeon-Joo Lee, Sooyeon Song, Boyong Kim, Hyuno Kang, Sejong Oh and Eungseok Kim

unexplored. The liver plays a key role in whole-body energy homeostasis by regulating lipogenesis and fatty acid oxidation ( Reddy & Rao 2006 ). A large body of evidence has shown that two transcription factors, sterol regulatory element-binding protein 1c

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Giselle Adriana Abruzzese, Maria Florencia Heber, Silvana Rocio Ferreira, Leandro Martin Velez, Roxana Reynoso, Omar Pedro Pignataro and Alicia Beatriz Motta

. Regarding fatty acid oxidation pathways, we found that Pparα mRNA levels showed no differences between the control and PHov groups but were decreased in PHanov ( Fig. 3H , P <0.01), and that Pgc1α levels were lower in both PH animals than in controls

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Andrea Anedda, Eduardo Rial and M Mar González-Barroso

present study was to determine whether UCP2 is involved in the action of metformin on white adipocytes. The working hypothesis was that UCP2 could be overexpressed either to uncouple respiration to facilitate fatty acid oxidation or to minimize the

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Jung-Yoon Heo, Ji-Eun Kim, Yongwook Dan, Yong-Woon Kim, Jong-Yeon Kim, Kyu Hyang Cho, Young Kyung Bae, Seung-Soon Im, Kwang-Hyeon Liu, In-Hwan Song, Jae-Ryong Kim, In-Kyu Lee and So-Young Park

fibrosis ( Jiang et al. 2005 b , Ishigaki et al. 2007 ). Fatty acid oxidation is one of the important energy-producing pathways in the kidney, particularly in the proximal tubules ( Mount et al. 2015 ). Fatty acids are usually bound to albumin in

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Jonathan M Mudry, Julie Massart, Ferenc L M Szekeres and Anna Krook

of the phosphorylated form of ACC was unchanged, leading to a larger ratio of inactivated ACC. In cultured C2C12 cells overexpressing TWIST1 or TWIST2, fatty acid oxidation in vitro was unchanged. Thus if glucose utilization is increased while fatty

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Amanda E Brandon, Ella Stuart, Simon J Leslie, Kyle L Hoehn, David E James, Edward W Kraegen, Nigel Turner and Gregory J Cooney

Acc2 knockout mice reported a lean phenotype with improved insulin action due to increased whole-body and muscle fatty acid oxidation (FAO) and higher energy expenditure ( Abu-Elheiga et al . 2001 , Abu-Elheiga et al . 2003 , Choi et al . 2007