2011
DOI: 10.1016/j.mce.2010.11.020
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Transcriptional co-factors and hepatic energy metabolism

Abstract: After binding to their cognate DNA-binding partner, transcriptional co-factors exert their function through the recruitment of enzymatic, chromatin-modifying activities. In turn, the assembly of co-factor-associated multi-protein complexes efficiently impacts target gene expression. Recent advances have established transcriptional co-factor complexes as a critical regulatory level in energy homeostasis and aberrant co-factor activity has been linked to the pathogenesis of severe metabolic disorders including o… Show more

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Cited by 14 publications
(10 citation statements)
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“…Hepatic metabolic adaptations leading to triglyceride accumulation (hepatosteatosis) and increased gluconeogenesis are primarily mediated by gene expression adjustments [15]. These alterations are frequently associated with aging and obesity and favor the development of systemic insulin resistance, the alteration of metabolic flexibility upon nutritional status changes [6].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Hepatic metabolic adaptations leading to triglyceride accumulation (hepatosteatosis) and increased gluconeogenesis are primarily mediated by gene expression adjustments [15]. These alterations are frequently associated with aging and obesity and favor the development of systemic insulin resistance, the alteration of metabolic flexibility upon nutritional status changes [6].…”
Section: Discussionmentioning
confidence: 99%
“…The development of hepatic insulin resistance is complex and involves several cofactors and regulatory pathways [15]. However, the contribution of SREBP-1c-dependent adaptations in hepatic metabolism was identified [16].…”
Section: Introductionmentioning
confidence: 99%
“…CRF, corticotrophin-releasing factor; ACTH, adrenocorticotrophin hormone; GLUT4, glucose transporter 4; IGF-1, insulin-like growth factor-1; AMPK, AMP kinase; LXR, liver X receptor; RXR, retinol X receptor; PEPCK, PEP carboxykinase; PKLR, pyruvate kinase; G6Pase, glucose-6-phosphatase; PGC1α, PPAR-γ co-activator-1; SRC-1, steroid receptor co-activator 1; CBP, CREB-binding protein; CREB, cAMP-response element binding protein; C/EBP, CCAAT/enhancer binding protein; GR, glucocorticoid receptor; GRE; glucocorticoid response element; HNF, hepatic nuclear factor; COUP, chicken ovalbumin upstream promotertranscription factor; FoxO1, foxhead box protein O1. determined by the physical recruitment and/or exchange of transcriptional co-activators/repressors to the GR, which have emerged as a critical regulatory layer in the control of tissue-specific and systemic energy homeostasis [52]. Indeed, during fasting, hepatic nuclear receptor co-factor peroxisome proliferator-activated receptor coactivator 1α (PGC-1α) [53] is activated in response to catecholamine/glucagon-triggered cAMP/cAMP responsive element binding protein (CREB) signaling [54].…”
Section: Gcs In Glucose Homeostasismentioning
confidence: 99%
“…Therefore it is very likely that disturbances in hepatic metabolism are linked to events contributing to the metabolic syndrome [91,92]. Several processes leading to a fatty liver phenotype are discussed.…”
Section: Lipid Metabolism and Nafldmentioning
confidence: 99%