Glucocorticoid Induced Whole Body Catabolisme
Whole Body Catabolisme Induced by Glucocorticoids
Drug: Calcium Supplement
|Study Design:||Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Basic Science
|Official Title:||Glucocorticoid Induced Inhibition of IGF-I Activity: Exploring Underlying Mechanisms.|
- Insulin-like Growth Factor (IGF)-I profiles of subjects before and after prednisolone-treatment. [ Time Frame: day 1, 3 and 5 ]Blood-test before (day 1) during (day 3) and at the end (day 5) of placebo/prednisolone treatment.
- Intracellular signaling of IGF-I under the influence/abscence of prednisolone. [ Time Frame: day 5 ]Tissue biopsy on day 5.
- Insulin sensitivity under the influence/abscence of prednisolone. [ Time Frame: Day 5 ]Hyperinsulinemic euglycemic clamp on day 5.
|Study Start Date:||January 2013|
|Study Completion Date:||June 2014|
|Primary Completion Date:||June 2014 (Final data collection date for primary outcome measure)|
Placebo Comparator: Calcium supplement
Capsule with tablet of calclium supplement
Drug: Calcium Supplement
Other Name: Placebo
Active Comparator: Glucocorticoids
Capsule with tablet of Prednisolone 37,5mg
Prednisolone 37.5 mg x1 for 5 days
Other Name: Prednisolone
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
Please refer to this study by its ClinicalTrials.gov identifier: NCT01762540
|Medical Research Laboratory, Clinical Institute of Medicine, Aarhus University Hospital|
|Aarhus, Denmark, 8000|
|Principal Investigator:||Jan Frystyk, Professor||Medical Research Laboratory, Clinical institute of Medicine, Aarhus University Hospital|