discusses the effects of cortisol on a bunch of things that we looked at (lipolysis, lipogenesis, muscle atrophy) and had gene expression data for some of these. I think based on this comment:
A recent paper by Morgan et al, PNAS showed that the 11beta HSD1 enzyme is an important mediator of mouse Cushing's and Dex is not HSD1 metabolised. Might this alter the profiles in mouse compared to using corticosterone?
We should discuss this paper in two contexts. One is to point out where their results support and/or contrast to our findings. The other is to mention something (a sentence or two) that addresses this question, specifically whether a) HSD11b1/2 can metabolize dex, with a reference and b) how you think the lack of local control of dex might affect our results. I think in the response we should include 11B-HSD1 mRNA levels from the mice (which i think you measured) and potentially do the enzyme assay (though i doubt that much effort is necessary)
This paper:
http://dx.doi.org/10.1073/pnas.1323681111
discusses the effects of cortisol on a bunch of things that we looked at (lipolysis, lipogenesis, muscle atrophy) and had gene expression data for some of these. I think based on this comment:
We should discuss this paper in two contexts. One is to point out where their results support and/or contrast to our findings. The other is to mention something (a sentence or two) that addresses this question, specifically whether a) HSD11b1/2 can metabolize dex, with a reference and b) how you think the lack of local control of dex might affect our results. I think in the response we should include 11B-HSD1 mRNA levels from the mice (which i think you measured) and potentially do the enzyme assay (though i doubt that much effort is necessary)