Preferential stimulation of abdominal subcutaneous lipolysis after prednisolone exposure in humans.
OBJECTIVE
The role of cortisol in the regulation of lipolysis is not clear. This study was undertaken to explore whether a standard dose of prednisolone for 1 week would influence lipolysis in abdominal and femoral tissue.


METHODS
We used the microdialysis technique, the forearm technique, and indirect calorimetry, in the fasting state, after 1 week of treatment with prednisolone (30 mg daily) or placebo. Eight healthy young men (age: 25 +/- 3 years; height: 181 +/- 1 cm; body mass index [BMI]: 23.3 +/- 0.7 kg/m(2)) were studied.


RESULTS
Treatment with prednisolone induced insulin resistance (Homeostasis Model Assessment index: placebo vs. prednisolone: 7.15 +/- 1.63 vs. 17.00 +/- 14.26, p = 0.03), hyperinsulinemia (p = 0.01), and hyperglucagonemia (p = 0.001), whereas growth hormone concentrations were unaffected. Abdominal adipose tissue interstitial glycerol was increased during treatment with prednisolone in the face of significant hyperinsulinemia, although it barely reached statistical significance (p = 0.06). At the femoral adipose tissue depot, no difference in lipolysis was found. Arterial and venous free fatty acids (FFA) were comparable in the two situations, whereas the arteriovenous difference across the forearm was significantly decreased during treatment with prednisolone, indicating increased uptake, or decreased release of FFA. Energy expenditure (p = 0.3), respiratory quotient (p = 0.9), glucose oxidation (p = 0.9), lipid oxidation (p = 1.0), and protein oxidation (p = 0.1) were unaltered on the 2 study days.


CONCLUSIONS
Short-term treatment with a standard dose of corticosteroids induces increased abdominal adipose tissue lipolysis, as well as hyperinsulinemia, hyperglucagonemia, and insulin resistance.
Medical Department M (Endocrinology and Diabetes) and Medical Research Laboratories, Arhus University Hospital, Arhus C, Denmark. ch.gravholt@dadlnet.dk
Claus Højbjerg
CH
Gravholt
Rolf
R
Dall
Jens Sandahl
JS
Christiansen
Niels
N
Møller
Ole
O
Schmitz
D000005:Abdomen / Q000098:blood supply; D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D002153:Calorimetry, Indirect; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004734:Energy Metabolism; D005215:Fasting; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005269:Femur; D005934:Glucagon / Q000097:blood; D005990:Glycerol / Q000378:metabolism; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008066:Lipolysis / Q000187:drug effects*; D008297:Male; D017551:Microdialysis; D010919:Placebos; D011239:Prednisolone / Q000494:pharmacology*
D001786:Blood Glucose; D002096:C-Peptide; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D010919:Placebos; D019382:Human Growth Hormone; D005934:Glucagon; D011239:Prednisolone; D005990:Glycerol