Wolthers T, Grøfte T, Nørrelund H, Poulsen P L, Andreasen F, Christiansen J S, Jørgensen J O
Medical Department M (Endocrinology and Diabetes), the Institute of Experimental Clinical Research, Aarhus University Hospital, Aarhus C, Denmark.
Metabolism. 1998 Jan;47(1):83-8. doi: 10.1016/s0026-0495(98)90197-4.
Short-term growth hormone (GH) exposure has been shown to stimulate energy expenditure (EE) without concomitant changes in body composition. To what extent this is related to thyroid function, sympathetic activity, hyperinsulinemia, or leptin secretion is unknown. It is also unknown whether the calorigenic effect of GH is influenced by glucocorticoids, which are known to antagonize the anabolic actions of GH. To pursue this, eight normal male subjects (aged 22 to 28 years; body mass index, 21.6 to 26.3 kg/m2) were randomly studied during four 4-day treatment periods with (1) daily subcutaneous (SC) placebo injections and placebo tablets, (2) daily SC GH injections (0.1 IU/kg x d) and placebo tablets, (3) daily prednisolone administration (25 mg morning and evening) plus placebo injections, and (4) daily GH injections plus prednisolone 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 leptin, 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, decreased norepinephrine (116 +/- 13, P < .05) and FT3 (4.7 +/- 0.2, P < .05), and increased leptin (3.93 +/- 0.71, P < .05). Concomitant GH and prednisolone administration increased REE (2,068 +/- 85, P +/- .05) and leptin (4.82 +/- 0.93, P +/- .05), had no effect on either epinephrine or norepinephrine, and decreased FT3 (5.0 +/- 0.2, P < .05). Resting heart rate (HR) increased only during GH, whereas sympathetic nerve activity was unchanged in all studies. Our data suggest that (1) the calorigenic effect of GH is not mediated by changes in sympathetic activity or leptin secretion, (2) rapid elevations in leptin induced by glucocorticoids do not affect EE in humans, and (3) the acute calorigenic effects of GH are probably related to increased cardiac workload.
短期生长激素（GH）暴露已被证明可刺激能量消耗（EE），而身体成分无相应变化。这种情况在多大程度上与甲状腺功能、交感神经活动、高胰岛素血症或瘦素分泌有关尚不清楚。GH的产热作用是否受糖皮质激素影响也不清楚，已知糖皮质激素会拮抗GH的合成代谢作用。为了探究这一点，八名正常男性受试者（年龄22至28岁；体重指数，21.6至26.3kg/m²）在四个为期4天的治疗期内被随机研究，分别为：（1）每日皮下（SC）注射安慰剂和口服安慰剂片；（2）每日SC注射GH（0.1IU/kg×d）和口服安慰剂片；（3）每日服用泼尼松龙（早晚各25mg）加安慰剂注射；（4）每日注射GH加服用泼尼松龙。注射GH显著降低了血浆肾上腺素（平均值±标准误，对照组为34.7±5.7ng/L，GH组为24.8±5.8，P<.05），对血浆去甲肾上腺素或血清瘦素无影响，并增加了游离三碘甲状腺原氨酸（FT3）水平（对照组为5.7±0.3pmol/L，GH组为6.7±0.3，P<.05）和静息能量消耗（[REE]对照组为1,861±61kcal/24h，GH组为1,996±69，P<.05）。服用泼尼松龙不影响肾上腺素和REE，降低了去甲肾上腺素（116±13，P<.05）和FT3（4.7±0.2，P<.05），并增加了瘦素（3.93±0.71，P<.05）。同时注射GH和服用泼尼松龙增加了REE（2,068±85，P±.05）和瘦素（4.82±0.93，P±.05），对肾上腺素或去甲肾上腺素均无影响，并降低了FT3（5.0±0.2，P<.05）。静息心率（HR）仅在注射GH期间增加，而在所有研究中交感神经活动均未改变。我们的数据表明：（1）GH的产热作用不是由交感神经活动或瘦素分泌的变化介导的；（2）糖皮质激素诱导的瘦素快速升高对人类的EE没有影响；（3）GH的急性产热作用可能与心脏工作负荷增加有关。
