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首页> 外文期刊>Frontiers in neuroendocrinology >Nutritional status in the neuroendocrine control of growth hormone secretion: the model of anorexia nervosa.
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Nutritional status in the neuroendocrine control of growth hormone secretion: the model of anorexia nervosa.

机译：营养状态在生长激素分泌的神经内分泌控制中：神经性厌食症模型。

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Growth hormone (GH) plays a key role not only in the promotion of linear growth but also in the regulation of intermediary metabolism, body composition, and energy expenditure. On the whole, the hormone appears to direct fuel metabolism towards the preferential oxidation of lipids instead of glucose and proteins, and to convey the energy derived from metabolic processes towards the synthesis of proteins. On the other hand, body energy stores and circulating energetic substrates take an important part in the regulation of somatotropin release. Finally, central and peripheral peptides participating in the control of food intake and energy expenditure (neuropeptide Y, leptin, and ghrelin) are also involved in the regulation of GH secretion. Altogether, nutritional status has to be regarded as a major determinant in the regulation of the somatotropin-somatomedin axis in animals and humans. In these latter, overweight is associated with marked impairment of spontaneous and stimulated GH release, while acutedietary restriction and chronic undernutrition induce an amplification of spontaneous secretion together with a clear-cut decrease in insulin-like growth factor I (IGF-I) plasma levels. Thus, over- and undernutrition represent two conditions connoted by GH hypersensitivity and GH resistance, respectively. Anorexia nervosa (AN) is a psychiatric disorder characterized by peculiar changes of the GH-IGF-I axis. In these patients, low circulating IGF-I levels are associated with enhanced GH production rate, highly disordered mode of somatotropin release, and variability of GH responsiveness to different pharmacological challenges. These abnormalities are likely due not only to the lack of negative IGF-I feedback, but also to a primary hypothalamic alteration with increased frequency of growth hormone releasing hormone discharges and decreased somatostatinergic tone. Given the reversal of the above alterations following weight recovery, these abnormalities can be seen as secondary, and possibly adaptive, to nutritional deprivation. The model of AN may provide important insights into the pathophysiology of GH secretion, in particular as regards the mechanisms whereby nutritional status effects its regulation.
机译：生长激素（GH）不仅在促进线性生长方面起着关键作用，而且在调节中间代谢，身体成分和能量消耗方面也起着关键作用。总体而言，该激素似乎将燃料代谢引导至脂质的优先氧化而不是葡萄糖和蛋白质，并且将代谢过程中产生的能量传递至蛋白质的合成。另一方面，人体能量存储和循环的能量底物在生长激素释放的调节中起着重要的作用。最后，参与食物摄入和能量消耗控制的中枢和外周肽（神经肽Y，瘦素和生长素释放肽）也参与GH分泌的调节。总之，营养状况必须被认为是调节动物和人类中生长激素-生长素轴的主要决定因素。在后者中，超重与自发性和刺激性GH释放明显受损有关，而急性饮食限制和慢性营养不良则导致自发性分泌增加，同时胰岛素样生长因子I（IGF-I）血浆水平明显降低。因此，营养过剩和营养不足分别代表GH超敏反应和GH抗药性所代表的两种情况。神经性厌食症（AN）是一种精神疾病，其特征是GH-IGF-1轴发生了特殊变化。在这些患者中，低循环的IGF-I水平与生长激素的产生速率增加，生长激素释放的高度紊乱模式以及生长激素对不同药理学挑战的反应性变化有关。这些异常可能不仅是由于缺乏IGF-I负反馈，而且还由于原发性下丘脑改变，其中生长激素释放激素释放的频率增加，而生长抑素能降低。考虑到体重减轻后上述改变的逆转，这些异常可以被认为是继发的，并且可能是对营养缺乏的适应。 AN模型可以为GH分泌的病理生理学提供重要见解，尤其是有关营养状况影响其调节的机制方面。

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