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. Author manuscript; available in PMC: 2013 Apr 16.
Published in final edited form as: Curr Opin Lipidol. 2009 Apr;20(2):98–105. doi: 10.1097/MOL.0b013e328328d0a4

Figure 1. A metabolic sensor network regulating energy expenditure.

Figure 1

Situations of energy depletion and/or decreased catabolic rates can be sensed by different enzymes, such as AMPK and SIRT1, whose activation enhance PGC-1α-dependent transcription. Upon calorie rich diets or situations when energy is not limited, AMPK activity is shut down by the high intracellular ATP levels. Similarly, high fat diets increase SRC-3, who positively regulates the protein levels of the acetyltransferase GCN5, which, in turn, plays the opposite role of SIRT1 action on PGC-1α acetylation, hence diminishing PGC-1α transcriptional activity. Perturbations in this metabolic network controlling PGC-1α activity may importantly contribute to whole-body metabolic complications.