Preferential stimulation of abdominal subcutaneous lipolysis after prednisolone exposure in humans
Preferential stimulation of abdominal subcutaneous lipolysis after prednisolone exposure in humans
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DOI：
10.1038/oby.2002.105
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发表时间：
2002-08-01
期刊：
影响因子：
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通讯作者：
Schmitz, O
中科院分区：
文献类型：
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作者：
Gravholt, CH;Dall, R;Schmitz, O
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.Research Methods and Procedures: 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), repiratory 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.Discussion: Short-term treatment with a standard dose of corticosteroids induces increased abdominal adipose tissue lipolysis, as well as hyperinsulinemia, hyperglucagonemia, and insulin resistance.
