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甲状腺状态和生长激素缺乏对胃饥饿素的影响。

Influence of thyroid status and growth hormone deficiency on ghrelin.

作者信息

Caminos J E, Seoane L M, Tovar S A, Casanueva F F, Dieguez C

机构信息

Department of Physiology, University of Santiago, Santiago de Compostela E-15700, Spain.

出版信息

Eur J Endocrinol. 2002 Jul;147(1):159-63. doi: 10.1530/eje.0.1470159.

Abstract

OBJECTIVE

To assess whether some of the alterations in energy homeostasis present in thyroid function disorders and GH deficiency could be mediated by ghrelin.

DESIGN

To assess the influence of thyroid status on ghrelin, adult male Sprague-Dawley rats were treated with vehicle (euthyroid), amino-triazole (hypothyroid) or l-thyroxine (hyperthyroid). The influence of GH on ghrelin was assessed in wild-type (control) and GH-deficient (dwarf) Lewis rats. Evaluation of gastric ghrelin mRNA expression in the stomach was carried out by Northern blot. Circulating levels of ghrelin were measured by radioimmunoassay.

RESULTS

Hypothyroidism resulted in an increase in gastric ghrelin mRNA levels (euthyroid: 100+/-3.2% vs hypothyroid: 127.3+/-6.5%; P<0.01), being decreased in hyperthyroid rats (70+/-5.4%; P<0.01). In keeping with these results, circulating plasma ghrelin levels were increased in hypothyroid (euthyroid: 124+/-11 pg/ml vs hypothyroid: 262+/-39 pg/ml; P<0.01) and decreased in hyperthyroid rats (75+/-6 pg/ml; P<0.01). Using an experimental model of GH deficiency, namely the dwarf rat, we found a decrease in gastric ghrelin mRNA levels (controls: 100+/-6% vs dwarf: 66+/-5.5%; P<0.01) and circulating plasma ghrelin levels (controls: 124+/-12 pg/ml vs dwarf: 81+/-7 pg/ml; P<0.01).

CONCLUSION

This study provides the first evidence that ghrelin gene expression is influenced by thyroid hormones and GH status and provides further evidence that ghrelin may play an important role in the alteration of energy homeostasis and body weight present in these pathophysiological states.

摘要

目的

评估甲状腺功能紊乱和生长激素缺乏时能量平衡的某些改变是否可由胃饥饿素介导。

设计

为评估甲状腺状态对胃饥饿素的影响,对成年雄性斯普拉格-道利大鼠分别给予溶媒(甲状腺功能正常)、氨基三唑(甲状腺功能减退)或左甲状腺素(甲状腺功能亢进)进行处理。在野生型(对照)和生长激素缺乏型(侏儒)刘易斯大鼠中评估生长激素对胃饥饿素的影响。通过Northern印迹法对胃中胃饥饿素mRNA表达进行评估。采用放射免疫分析法测定循环中胃饥饿素水平。

结果

甲状腺功能减退导致胃饥饿素mRNA水平升高(甲状腺功能正常:100±3.2% vs甲状腺功能减退:127.3±6.5%;P<0.01),而在甲状腺功能亢进大鼠中降低(70±5.4%;P<0.01)。与这些结果一致,甲状腺功能减退大鼠循环血浆胃饥饿素水平升高(甲状腺功能正常:124±11 pg/ml vs甲状腺功能减退:262±39 pg/ml;P<0.01),而在甲状腺功能亢进大鼠中降低(75±6 pg/ml;P<0.01)。利用生长激素缺乏的实验模型,即侏儒大鼠,我们发现胃饥饿素mRNA水平降低(对照:100±6% vs侏儒:66±5.5%;P<0.01)以及循环血浆胃饥饿素水平降低(对照:124±12 pg/ml vs侏儒:81±7 pg/ml;P<0.01)。

结论

本研究首次证明胃饥饿素基因表达受甲状腺激素和生长激素状态影响,并进一步证明胃饥饿素可能在这些病理生理状态下的能量平衡和体重改变中起重要作用。

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