Fig. 1.

Fig. 1. : 

Transcriptional control of glycolysis and lipogenesis. The conversion of glucose into fatty acids through de novo lipogenesis is nutritionally regulated, and both glucose and insulin signaling pathways are elicited in response to dietary carbohydrates to synergistically induce glycolytic and lipogenic gene expression. The nature of the glucosesignaling compound was recently identified as the transcription factor ChREBP (carbohydrate responsive element-binding protein). Glucose activates ChREBP by stimulating its gene expression and mediating its post-translational modification(s). ChREBP is required for the induction of L-PK, which is exclusively dependent on glucose. Induction of lipogenic genes, such as ACC, FAS, SCD-1, is under the combined actions of ChREBP and SREBP-1c. Transcription factor SREBP-1c also mediates the effect of insulin on GPAT, although the direct action of ChREBP on GPAT gene expression has not been established. As the nuclear receptor LXR is required for insulin action on SREBP-1c expression, insulin must, in some manner, stimulate the production of an endogenous sterol ligand of LXR (oxysterols). ChREBP is also a direct target of LXR when activated by pharmacological agonists such as T0-901317, but LXR is unable to activate ChREBP expression in response to glucose (Adapted from Robichon et al . [54]).