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

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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.”
A practical model of low‐volume high‐intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms (2010, background): “Although SIRT1 has been primarily recognized as a positive regulator of mitochondrial biogenesis (Rodgers et al. 2005; Civitarese et al. 2007; Canto et al. 2009; Gerhart-Hines et al. 2007; Suwa et al. 2008), recent data from Gurd and colleagues (2009) has challenged this view.”
Therapeutic potential of NAD-boosting molecules: the in vivo evidence (2018, neutral): “SIRT1 and its downstream targets PGC-1a, PSK9, and SREBP1 maintain mitochondrial function, cholesterol transport, and fatty acid homeostasis (Baur et al., 2006; Picard et al., 2004; Rodgers et al., 2005; Yang et al., 2006).”
Transcriptional control of adipocyte formation. (2006, background): “SIRT1 is a NAD-dependent protein deacetylase capable of monitoring cellular oxidative state and altering the activity of nuclear regulators in response to metabolites and nutrients (Imai et al., 2000; Rodgers et al., 2005).”