AMPK and PPARd Agonists Are Exercise Mimetics

By V. Narkar, M. Downes, R. Yu, Emi Embler, Yong-Xu Wang, Ester Banayo, Maria M. Mihaylova, Michael C. Nelson, Yuhua Zou, Henry Juguilon and 3 more. 2008

1,087 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9cf436d295a62476ca13986d2c384ef90409d362

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The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. R. Shaw
2. D. Hardie
3. Keisuke Ito
4. T. Suda
5. Arkaitz Carracedo
6. Bei B. Zhang
7. Gerald I. Shulman
8. F. Jornayvaz

Citations in the corpus

• Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “…mice (Wang et al., 2004; Calvo et al., 2008; Garcia-Roves et al., 2008), or similar effects produced pharmacologically (Lagouge et al., 2006; Narkar et al., 2008), has ignited interest in developing so-called exercise ‘‘mimetics,’’ i.e., pharmacotherapy to replicate the metabolic effects of…”
• The AMP-activated protein kinase (AMPK) signaling pathway coordinates cell growth, autophagy, & metabolism (2011, background): “Interestingly, AMPK was also implicated in skeletal muscle reprogramming in a study where sedentary mice were treated with AICAR for 4 weeks and were found to be able to perform 44% better than counterparts that received control vehicl”
• Transcriptional control of mitochondrial biogenesis and function. (2009, background): “The importance of parallel pathways is nicely demonstrated in a recent study showing that, although pharmacological activation of PPARδ by itself does not enhance exercise performance, the combination of the PPARδ agonist with exercise training results in the synergistic enhancement of exercise perf”
• Regulation of mitochondrial biogenesis (2010, background): “It has been shown recently that the AMPK agonist AICAR can increase endurance in sedentary mice by genetically reprogramming muscle metabolism [21].”
• Integrative biology of exercise. (2014, unknown): “Consequently, given the numerous benefits of exercise on general health, it has been stated that ‘‘the identification of genetic and/or orally active agents that mimic or potentiate the effects of endurance exercise is a longstanding albeit elusive medical goal’’ (Narkar et al., 2008).”
• Metabolic flexibility in health and disease (2017, unknown): “Pharmacological activation of AMPK alters the expression of many of the same genes seen with exercise (Narkar et al., 2008).”
• AMPK: an emerging drug target for diabetes and the metabolic syndrome. (2009, background): “Indeed, 4 weeks of AICAR treatment was sufficient to induce genes involved in muscle metabolism and to enhance running endurance in sedentary mice (Narkar et al., 2008).”
• AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. (2011, background): “2000) or mice (Narkar et al. 2008), led to the up-regulation of nuclear-encoded mitochondrial genes and, in the mouse study, improved endurance in treadmill running tests.”
• A PML-PPARδ pathway for fatty acid oxidation regulates haematopoietic stem cell maintenance (2012, background): “The PML (promyelocytic leukemia) tumor-suppressor gene, originally cloned at the break point of the t(15;17) chromosomal translocation of acute promyelocytic leukemia, has a key role in the maintenance of HSCs16.”
• LKB1 and AMPK control of mTOR signalling and growth (2009, background): “In skeletal muscle, AMPK activation has been shown to promote mitochondrial biogenesis at least in part through transcription effects downstream of PPARgamma coactivator (PGC)-1a and peroxisome proliferator-activated receptor (PPAR)-d (Jager et al. 2007, Narkar et al. 2008).”