Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt.
By M. Fulco, Yana Cen, Po Zhao, Eric P. Hoffman, M. McBurney, A. Sauve, V. Sartorelli. Developmental Cell, 2008
820 citations recorded by the source corpus.
Subfields: Epidemiology, Geriatrics and Gerontology, Physiology
View Paper: https://www.semanticscholar.org/paper/81600f1a8523244f749b224db8c327f5a58bdbfe
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Citations in the corpus
- SIRT1 and other sirtuins in Metabolism (2013, background): “AMPK can increase NAD+ levels by up-regulating NAMPT (nicotinamide phosphoribosyltransferase), one of the crucial enzymes for NAD biosynthesis [78,79].”
- Sirtuin 1 modulates cellular responses to hypoxia by deacetylating hypoxia-inducible factor 1alpha. (2010, background): “In all cells tested, intracellular NAD+ level and NAD+/NADH ratio significantly decreased in a hypoxic time-dependent manner (Figure 5F; Figure S7A, available online).”
- Resveratrol Ameliorates Aging-Related Metabolic Phenotypes by Inhibiting cAMP Phosphodiesterases (2012, neutral): “[PubMed: 9856955] Lagouge M, Argmann C, Gerhart-Hines Z, Meziane H, Lerin C, Daussin F, Messadeq N, Milne J, Lambert P, Elliott P, et al. Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha.”
- The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. (2010, background): “Similarly, NAD content increases by more than 100% in cultured myotubes upon glucose deprivation (85, 96), and around 45% in fasted muscle (C.”
- SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “This model is not consistent with the effects we have observed with moderate doses of resveratrol in vitro or in vivo, as increases in p-AMPK, NAD+, LKB1 acetylation, and mitochondrial function were entirely SIRT1dependent.”
- NAD+ metabolism and the control of energy homeostasis - a balancing act between mitochondria and the nucleus (2015, background): “, 2005), or low glucose availability (Fulco et al., 2008), all of which correlate with higher NAD levels.”
- Mitochondrial Dysfunction in Neurodegenerative Diseases (2012, background): “PGC-1␣ activity is modulated by SIRT1, an NAD-dependent deacetylase, and activation of SIRT1 is protective in models of HD (Jeong et al., 2012; Jiang et al., 2012).”
- Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice (2011, background): “528 Cell Metabolism 14, 528–536, October 5, 2011 a2011 Elsevier In For example, in skeletal muscle, both nutritional deprivation and exercise increase Nampt expression through the activation of AMP-activated protein kinase (AMPK), thereby enhancing NAD biosynthesis and SIRT1 activity (Cantó et al., ”
- Caloric restriction. (2011, background): “Fourth it activates SIRT-1 via the NAD synthetic enzyme nicotinamide phosphoribosyltransferase (NamPT) (Fulco et al., 2008) and finally it promotes mitochondrial biogenesis.”
- Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle (2010, background): “AMPK enhances SIRT1 activity by increasing intracellular NAD levels (Canto et al., 2009; Costford et al., 2009; Fulco et al., 2008).”