Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1.

By J. T. Rodgers, C. Lerín, W. Haas, Steven P. Gygi, B. Spiegelman, P. Puigserver. Nature, 2005

1,465 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/796e1100239eb12f28a8c9a445099fcb46666497

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Citations in the corpus

Sirtuin 3, a New Target of PGC-1α, Plays an Important Role in the Suppression of ROS and Mitochondrial Biogenesis (2010, background): “Previous studies have suggested SIRT1 directly interacts with and deacetylates transcriptional coactivator PGC-1a [42,48].”
Sirt1 protects against high-fat diet-induced metabolic damage (2008, background): “Both genes, MnSOD and Nrf1, have been demonstrated to be induced by PGC1 (28), which in turn is positively regulated by Sirt1 (10, 13).”
Sirtuins in aging and age-related disease. (2006, background): “Sirt1 also induces gluconeogenic genes and hepatic glucose output through the transcriptional coactivator PGC-1 α (Rodgers et al., 2005).”
Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “SirT1 associates with PGC-1α in the central regulatory region between amino acids 200 and 400 and deacetylates PGC-1α, leading to enhanced transcriptional activity in a NAD+-dependent way (Rodgers et al., 2005).”
Energy Metabolism in the Liver (2014, unknown): “SIRT1 deacetylates PGC-1α, thus increasing its ability to coactivate HNF-4α for gluconeogenesis (226).”
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine (2005, background): “HNF-4α, a member of the steroid/thyroid hormone receptor superfamily, acts as an upstream regulator of HNF-1α (231).”
Reprogramming of the Circadian Clock by Nutritional Challenge (2013, unknown): “The lack of circadian NAD+ accumulation under HFD supports the observation that NAD+ is high during fasting (Rodgers et al., 2005).”
Redox regulation of FoxO transcription factors (2015, background): “In response to fasting signals, Sirt1 deacetylates both FoxO1a and PGC-1α in hepatocytes, resulting in increased transcription of gluconeogenic genes and elevated glucose release from the liver [104,110].”
NAD+ metabolism and the control of energy homeostasis - a balancing act between mitochondria and the nucleus (2015, background): “For example, SIRT1 activity increases during exercise (Cantó et al., 2009), CR (Chen et al., 2008), fasting (Cantó et al., 2010; Rodgers et al., 2005), or low glucose availability (Fulco et al., 2008), all of which correlate with higher NAD+ levels.”
SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis (2007, background): “In accordance with increased protein levels of SIRT1, there was a decrease in the acetylation state of PGC-1alpha, a target for SIRT1 deacetylase activity (Nemoto et al, 2005; Rodgers et al, 2005; St-Pierre et al, 2006) (Figure 1C).”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, unknown): “The NAD þ -dependent histone deacetylase, SIRT1 increases gluconeogenesis in liver cells through its effects on PGC-1 a (272).”
The NAD+-Dependent Deacetylase SIRT1 Modulates CLOCK-Mediated Chromatin Remodeling and Circadian Control (2008, unknown): “, 2004), and mediates the metabolism of energy sources in metabolically active tissues (Lagouge et al., 2006; Rodgers et al., 2005).”
Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice (2008, unknown): “We first examined expression of several SIRT1 downstream genes, including G6pase, Pepck, and Pgc-1a (Lagouge et al., 2006; Rodgers et al., 2005).”
Hepatocyte-specific Deletion of SIRT1 Alters Fatty Acid Metabolism and Results in Hepatic Steatosis and Inflammation (2009, unknown): “PGC-1a is a direct substrate of SIRT1, and deacetylation of this coactivator by SIRT1 stimulates its activity (Rodgers et al., 2005).”
The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity (2012, unknown): “We also evaluated PGC-1α acetylation as a second readout of SIRT1 activity (Rodgers et al., 2005).”
Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies (2016, background): “In energy deprived state, AMPK and SIRT1 regulate PGC-1α through phosphorylation and deacetylation, respectively [61].”