title: Energetic cell sensors: a key to metabolic homeostasis.
abstract: Recent breakthrough studies suggest that metabolic signals such as AMP/NAD(+) and acetyl-CoA during fasting and feeding, respectively, translate the energetic cell status into specific transcriptional metabolic programs. Notably, NAD(+) and acetyl-CoA modulate chromatin packaging and gene expression as substrates of histone deacetylases or histone acetyltransferases, respectively. These energetic sensors regulate circadian rhythms and their related physiological processes. In addition, NAD(+) indirectly activates peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) during fasting, whereas acetyl-CoA inactivates PGC-1alpha upon feeding. In this review, we focus on recent evidence supporting the concept of an energetic code by which metabolic sensors control homeostasis during fasting and feeding and discuss its relevance to the pathophysiology of type 2 diabetes.
authors.affiliation: INSERM, U907, Nice F-06107, France.
authors.forename: Mourad
authors.initials: M
authors.lastname: Naïmi
authors.forename: Caroline
authors.initials: C
authors.lastname: Arous
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Van Obberghen
mesh_terms: D000105:Acetyl Coenzyme A / Q000378:metabolism / Q000502:physiology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000263:Adenylate Kinase / Q000378:metabolism; D000818:Animals; D002468:Cell Physiological Phenomena; D002477:Cells / Q000378:metabolism*; D004435:Eating / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D005215:Fasting / Q000378:metabolism / Q000502:physiology; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D037761:Sirtuins / Q000378:metabolism / Q000502:physiology
chemical_list: D000105:Acetyl Coenzyme A; D000255:Adenosine Triphosphate; D000263:Adenylate Kinase; D037761:Sirtuins