The glucocorticoid receptor represses, whereas C/EBPβ can enhance or repress CYP26A1 transcription

Energy status regulates levels of the RAR/RXR ligand 9-cis-retinoic acid in mammalian tissues: Glucose reduces its synthesis in β-cells

“…Fasting decreased 9cRA ∼50% in the kidney. Fasting increased atRA ∼1.9-fold in the liver, consistent with previous reports ( 40 , 41 , 42 ). Fasting/refeeding did not affect atRA levels in serum, BAT, iWAT, kidney, brain, and testis.…”

“…Tissues express Rdh5 widely and recombinant Rdh5 catalyzes conversion of 9- cis -retinol into 9cRA efficiently ( 46 ). Decreases in 9- cis -retinal and 9cRA with 15 mM glucose suggest that refeeding versus fasting affects Rdh5 mRNA or Rdh5 activity, as it does for Rdh1 and Rdh10 in the liver ( 40 , 41 , 42 ). Refeeding after a fast decreased Rdh5 mRNA in pancreas, with reductions of 40 and 67% in 4 and 6 h, respectively ( Fig.…”

“…Suppression of RAR by alternative mechanism(s) might also occur. For example, the glucocorticoid receptor represses RA-induced transcription by interacting with the RAR/RXR transcription complex ( 41 ). Finally, with respect to a role for 9cRA as a signaling molecule, it has at least 5-fold higher affinity for RAR than RXR ( 88 ).…”

Dissecting the Long-Term Effect of Stress Early in Life on FKBP5: The Role of miR-20b-5p and miR-29c-3p

“…Interestingly, upon testing for gene x environment (GxE) interactions in two Genome wide association studies (GWAS) samples of adult controls and depressed patients exposed to childhood traumatic experiences, FoxO1 has been confirmed to be a stress responsive gene, able to mediate the effect of the environment on the development of depressive symptoms [ 14 ]. Accordingly, FoxO1 has been found to be able to mediate the effect of GCs in other disorders, including cancer [ 15 ] and insulin resistance [ 16 , 17 ].…”

“…Interestingly, upon testing for gene x environment (GxE) interactions in two Genome wide association studies (GWAS) samples of adult controls and depressed patients exposed to childhood traumatic experiences, FoxO1 has been confirmed to be a stress responsive gene, able to mediate the effect of the environment on the development of depressive symptoms [14]. Accordingly, FoxO1 has been found to be able to mediate the effect of GCs in other disorders, including cancer [15] and insulin resistance [16,17]. Although ELS exposure can contribute to the onset of psychopathology or to the development of clinical symptoms later in life, through the involvement of stress-responsive genes, the underlying and long-lasting GR-dependent mechanisms induced by ELS are still unclear.…”