here also supports a potential role for the GR in regulating SEPP1 expression. Glucocorticoid responsiveness of SEPP1 could be of significance in critically ill patients, as these patients tend to have increased levels of free plasma cortisol levels (Hamrahian et al. 2004). Such regulation of SEPP1 by glucocorticoids could serve as an alternative explanation for the changes in SelP, and therefore the changes in serum selenium levels, observed during critical illness. However, a recent study demonstrates that the decrease in SelP in the acute-phase response appears to be a deficit in translation rather than a transcriptional response (Renko et al. 2009); therefore, the data herein may be more relevant for development or differentiation.
