DIFFERENTIAL-EFFECTS OF GROWTH-HORMONE AND PREDNISOLONE ON ENERGY-METABOLISM AND LEPTIN LEVELS IN HUMANS

Short-term growth hormone (GH) exposure has been shown to stimulate en ergy expenditure (EE) without concomitant changes in body composition. To what extent this is related to thyroid function, sympathetic activ ity, hyperinsulinemia, or leptin secretion is unknown. It is also unkn own whether the calorigenic effect of GH is influenced by glucocortico ids, which are known to antagonize the anabolic actions of GH. To purs ue this, eight normal male subjects (aged 22 to 28 years; body mass in dex, 21.6 to 26.3 kg/m(2)) were randomly studied during four 4-day tre atment periods with ill daily subcutaneous (SC) placebo injections and placebo tablets, (2) daily SC GH injections (0.1 lU/kg.d) and placebo tablets, (3) daily prednisolone administration (25 mg morning and eve ning) plus placebo injections, and (4) daily GH injections plus predni solone administration. GH administration decreased plasma epinephrine significantly (mean +/- SE, 34.7 +/- 5.7 ng/L for control v 24.8 +/- 5 .8 for GH, P < .05), had no effect on plasma norepinephrine or serum l eptin, and increased both free triiodothyronine (FT3) levels (5.7 +/- 0.3 pmol/L for control v 6.7 +/- 0.3 for GH, P < .05) and resting EE ( [REE] 1,861 +/- 61 kcal/24 h for control v 1,996 +/- 69 for GH, P <.05 ). Prednisolone administration did not affect epinephrine and REE, dec reased norepinephrine (116 +/- 13, P < .05) and FT3 (4.7 +/- 0.2, P < .05), and increased leptin (3.93 +/- 0.71, P < .05). Concomitant GH an d prednisolone administration increased REE (2,068 +/- 85, P +/- .05) and leptin (4.82 +/- 0.93, P +/- .05), had no effect on either epineph rine or norepinephrine, and decreased FT3 (5.0 +/- 0.2, P < .05). Rest ing heart rate (HR) increased only during GH, whereas sympathetic nerv e activity was unchanged in all studies. Our data suggest that (1) the calorigenic effect of GH is not mediated by changes in sympathetic ac tivity or leptin secretion, (2) rapid elevations in leptin induced by glucocorticoids do not affect EE in humans, and (3) the acute calorige nic effects of GH are probably related to increased cardiac workload. Copyright (C) 1998 by W.B. Saunders Company.