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Additive effects of cortisol and growth hormone on regional and systemic lipolysis in humans

¹Department of Endocrinology and Diabetes, University Hospital of Aarhus, Aarhus Kommunehospital; ²Institute of Experimental Clinical Research, and ³Institute of Clinical Pharmacology, University of Aarhus; and ⁴Department of Endocrinology and Metabolism, University Hospital of Aarhus, Aarhus Amtssygehus DK-8000 Aarhus, Denmark

Submitted 2 May 2003 ; accepted in final form 13 October 2003

Growth hormone (GH) and cortisol are important to ensure energy supplies during fasting and stress. In vitro experiments have raised the question whether GH and cortisol mutually potentiate lipolysis. In the present study, combined in vivo effects of GH and cortisol on adipose and muscle tissue were explored. Seven lean males were examined four times over 510 min. Microdialysis catheters were inserted in the vastus lateralis muscle and in the subcutaneous adipose tissue of the thigh and abdomen. A pancreatic-pituitary clamp was maintained with somatostatin infusion and replacement of GH, insulin, and glucagon at baseline levels. At t = 150 min, administration was performed of NaCl (I), a 2 µg·kg^-1·min^-1 hydrocortisone infusion (II), a 200-µg bolus of GH (III), or a combination of II and III (IV). Systemic free fatty acid (FFA) turnover was estimated by [9,10-³H]palmitate appearance. Circulating levels of glucose, insulin, and glucagon were comparable in I-IV. GH levels were similar in I and II (0.50 ± 0.08 µg/l, mean ± SE). Peak levels during III and IV were 9 µg/l. Cortisol levels rose to 900 nmol/l in II and IV. Systemic (i.e., palmitate fluxes, s-FFA, s-glycerol) and regional (interstitial adipose tissue and skeletal muscle) markers of lipolysis increased in response to both II and III. In IV, they were higher and equal to the isolated additive effects of the two hormones. In conclusion, we find that GH and cortisol stimulate systemic and regional lipolysis independently and in an additive manner when coadministered. On the basis of previous studies, we speculate that the mode of action is mediated though different pathways.

microdialysis; corticosteroids

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