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Endocrine Abstracts (2014) 34 S2.1 | DOI: 10.1530/endoabs.34.S2.1

University of Birmingham, Birmingham, UK.


Current dogma suggests that glucocorticoids (GCs) cause insulin resistance in all tissues. Whilst it is clear that they cause global, whole body insulin resistance, we have challenged the concept that the actions of GCs are the same in all tissues. Using a variety of human cell-based models, we have shown that in contrast to their actions in skeletal muscle and liver, GCs cause insulin sensitization in human adipose tissue, enhancing insulin-stimulated PKB/akt phosphorylation, glucose uptake, and lipogenesis. Whilst these effects persist for up to 7 days, there are, in addition, depot specific differences; our observations seem confined to the subcutaneous adipose tissue depot. In omental cells, GCs cause neither insulin sensitization, nor insulin resistance. Whilst it is possible that our observations reflect in vitro culture systems, we have recently extended our findings to a translational randomized, double blind, placebo controlled, cross-over study. Patients were treated with either overnight hydrocortisone or saline infusions in a random order. Following GC treatment, we observed hepatic and skeletal muscle insulin resistance, however, insulin-mediated suppression of adipose tissue lipolysis was enhanced, as was insulin-stimulated pyruvate generation. These data that are consistent with adipose tissue insulin sensitization.

Our studies have demonstrated opposing metabolic actions of GCs that challenge current textbook definitions and highlight the importance of tissue-specific assessments in clinical studies.

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