Insulin-regulated hepatic gluconeogenesis through FOXO1-PGC-1alpha interaction.

By P. Puigserver, James Rhee, Jerry Donovan, C. Walkey, J. C. Yoon, F. Oriente, Y. Kitamura, J. Altomonte, Hengjiang Dong, D. Accili and 1 more. Nature, 2003

713 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/41079d5e2a3a16160dcbfe9aa0d339244d016e60

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Citations in the corpus

Impaired regulation of hepatic glucose production in mice lacking the forkhead transcription factor Foxo1 in liver. (2007, methodology): “The forkhead transcription factor Foxo1 confers insulin responsiveness onto G6pc expression (Nakae et al., 2001) by interacting with Pgc1a (Puigserver et al., 2003).”
The role of FoxO in the regulation of metabolism (2008, background): “Oncogene promoter; dominant-inhibitory FoxO1 blunts PGC1ainduced PEPCK expression (Puigserver et al., 2003).”
Regulation of energy metabolism by long-chain fatty acids. (2014, background): “FOXO1 is a transcription factor involved in regulation of cell cycle and cellular metabolism [140].”
Suppression of reactive oxygen species and neurodegeneration by the PGC-1 transcriptional coactivators. (2006, background): “…adaptive thermogenesis in brown adipose tissue (BAT) (Puigserver et al., 1998), fiber-type switching in skeletal muscle (Lin et al., 2002), and both b-oxidation of fatty acids and gluconeogenesis in liver (Herzig et al., 2001; Puigserver et al., 2003; Rhee et al., 2003; Yoon et al., 2001).”
Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism (2010, unknown): “Consistent with these results, phosphorylation of InsR on tyrosines 1150 and 1151 and of FoxO1, a target of insulin signaling (Puigserver et al., 2003), was increased in Esp À/À osteoblasts (Figure 1H and Figures S1I and S1J).”
FoxO3 controls autophagy in skeletal muscle in vivo. (2007, background): “In fact, the increased muscle protein catabolism induced by FoxO3 contributes amino acids that are used for glucose production by the liver, where FoxO1 has been shown to control gluconeogenesis gene expression (Puigserver et al., 2003).”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “Transcription factor targets of the PGC-1 coactivators Transcription factor PGC-1α PGC-1β Function References NRF-1 + + mitochondrial genes Wu et al., 1999 NRF-2 + ND mitochondrial genes Mootha et al., 2003 PPARα + + fatty-acid oxidation Vega et al., 2000 PPARβ/δ + ND fatty-acid oxidation Wang et al”
Cellular and molecular mechanisms of muscle atrophy (2013, unknown): “…from denervation-induced atrophy Hishiya et al., 2006 Autophagy-lysosome Atg5 Muscle-specific KO Muscle weakness, atrophy, myopathic phenotype Raben et al., 2008 Atg7 Muscle-specific KO, inducible muscle-specific KO Muscle weakness, atrophy, myopathic phenotype, increased muscle loss during…”
Redox regulation of FoxO transcription factors (2015, background): “PGC-1α is a positive regulator of fasting-induced hepatic gluconeogenesis and this is mediated through its interaction with FoxO1a [200].”
The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “[15] Pyper SR, Viswakarma N, Yu S, Reddy JK. PPARalpha: energy combustion, hypolipidemia, inflammation and cancer.”