AI Article Synopsis
- Recent research indicates that metabolic signals like AMP/NAD(+) during fasting and acetyl-CoA during feeding communicate the cell's energy status to specific metabolic programs.
- These signals influence gene expression and chromatin structure, affecting how genes are activated or deactivated via histone modifications.
- The review highlights how these metabolic sensors help regulate body rhythms and have implications for understanding type 2 diabetes.
Article 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.
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| http://dx.doi.org/10.1016/j.tem.2009.09.003 | DOI Listing |
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