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生长激素的代谢作用:直接和间接作用

Metabolic actions of growth hormone: direct and indirect.

作者信息

Berneis K, Keller U

机构信息

Department of Research, Metabolic Unit, Kantonsspital, Basel, Switzerland.

出版信息

Baillieres Clin Endocrinol Metab. 1996 Jul;10(3):337-52. doi: 10.1016/s0950-351x(96)80470-8.

DOI:10.1016/s0950-351x(96)80470-8
PMID:8853443
Abstract

GH may exert metabolic effects either directly or indirectly through increased production of IGF-I. GH administration increases circulating IGF-I levels via stimulation of hepatic synthesis and secretion of IGF-I; it may also enhance local IGF-I synthesis, which exerts paracrine or autocrine effects. Figure 2 summarizes the metabolic effects of GH and IGF-I. Administration of GH and IGF-I in adult humans has been demonstrated to enhance protein anabolism. Combined administration of GH and IGF-I was observed to be more anabolic than either IGF-I or GH alone. Evidence is presented that protein accretion results mainly from direct effects of GH on tissues; additional indirect effects via IGF-I production are also likely. Administration of GH has been reported to produce carbohydrate intolerance with elevated plasma insulin levels, resulting from insulin resistance. in contrast, insulin sensitivity increased during administration of IGF-I, which exerts hypoglycaemic effects even with concomitant suppression of insulin secretion. A major direct metabolic effect of GH is to increase fat mobilization and oxidation, and thereby to reduce total body fat; there is no evidence that IGF-I acts directly on adipose tissue in vivo. GH administration results in sodium retention via stimulation of Na-K-ATPase. It is suggested that part of the effects of GH on tubular function (e.g. phosphate reabsorption) are mediated via IGF-I. Energy expenditure may be increased by administration of either GH or relatively high doses of IGF-I. One of the reasons for this phenomenon is an increase in lean body mass; GH may increase energy expenditure additionally be enhancing the production of T3 and by increasing lipid oxidation.

摘要

生长激素(GH)可直接或通过增加胰岛素样生长因子-1(IGF-I)的产生间接发挥代谢作用。给予生长激素可通过刺激肝脏合成和分泌IGF-I来提高循环中的IGF-I水平;它还可能增强局部IGF-I的合成,从而发挥旁分泌或自分泌作用。图2总结了生长激素和IGF-I的代谢作用。在成年人体内给予生长激素和IGF-I已被证明可增强蛋白质合成代谢。观察到生长激素和IGF-I联合给药比单独使用IGF-I或生长激素更具合成代谢作用。有证据表明蛋白质蓄积主要源于生长激素对组织的直接作用;通过IGF-I产生的额外间接作用也很可能存在。据报道,给予生长激素会导致碳水化合物不耐受,同时血浆胰岛素水平升高,这是由胰岛素抵抗引起的。相比之下,在给予IGF-I期间胰岛素敏感性增加,即使在胰岛素分泌受到抑制的情况下,IGF-I也会发挥降血糖作用。生长激素的一个主要直接代谢作用是增加脂肪动员和氧化,从而减少全身脂肪;没有证据表明IGF-I在体内直接作用于脂肪组织。给予生长激素会通过刺激钠钾ATP酶导致钠潴留。有人认为生长激素对肾小管功能(如磷酸盐重吸收)的部分作用是通过IGF-I介导的。给予生长激素或相对高剂量的IGF-I可能会增加能量消耗。这种现象的一个原因是瘦体重增加;生长激素可能还会通过增强三碘甲状腺原氨酸的产生和增加脂质氧化来增加能量消耗。

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