The main purpose of the trial is to advance our knowledge on the possible mechanism underlying the catabolic effects of long-term treatment with glucocorticoid.
Long-term treatment with glucocorticoid induces a general state of catabolism and increases insulin resistance. The underlying mechanisms are insufficiently characterized, however glucocorticoid induced changes of Growth Hormone (GH) and the Insulin-like growth factor I (IGF-I) appear to be of outmost importance. We wish to investigate the mechanism behind glucocorticoid induced catabolism and insulin resistance. More specific we wish to investigate: * Whether glucocorticoid induces IGF-I inhibiting substances in serum or interstitial fluid that block the ability of IGF-I to phosphorylate its receptor in vitro * Whether glucocorticoid inhibits intracellular IGF-I and insulin signaling in vitro and in vivo * The mechanisms by which growth hormone counteracts the CG-mediated inhibition of IGF-I action
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
QUADRUPLE
Enrollment
19
Prednisolone 37.5 mg x1 for 5 days
Placebo
Medical Research Laboratory, Clinical Institute of Medicine, Aarhus University Hospital
Aarhus, Denmark
Insulin-like Growth Factor (IGF)-I profiles of subjects before and after prednisolone-treatment.
Blood-test before (day 1) during (day 3) and at the end (day 5) of placebo/prednisolone treatment.
Time frame: day 1, 3 and 5
Intracellular signaling of IGF-I under the influence/abscence of prednisolone.
Tissue biopsy on day 5.
Time frame: day 5
Insulin sensitivity under the influence/abscence of prednisolone.
Hyperinsulinemic euglycemic clamp on day 5.
Time frame: Day 5
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