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短期热量限制对肥胖受试者循环游离胰岛素样生长因子-I、酸不稳定亚基、胰岛素样生长因子结合蛋白(IGFBPs)-1 - 4以及IGFBPs - 1 - 3蛋白酶活性的影响。

Effects of short-term caloric restriction on circulating free IGF-I, acid-labile subunit, IGF-binding proteins (IGFBPs)-1-4, and IGFBPs-1-3 protease activity in obese subjects.

作者信息

Rasmussen Michael Højby, Juul Anders, Kjems Lise Lund, Hilsted Jannik

机构信息

Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, DK-2650 Copenhagen, Denmark.

出版信息

Eur J Endocrinol. 2006 Oct;155(4):575-81. doi: 10.1530/eje.1.02246.

DOI:10.1530/eje.1.02246
PMID:16990657
Abstract

OBJECTIVE

Decreased levels of GH and total IGF-I have been reported in obesity. It has been hypothesized that increased free (biologically active) IGF-I levels generated from IGF-binding protein (IGFBP) protease activity could be the mechanism for the low GH release in dieting obese subjects. However, no published data exist on free IGF-I levels, acid labile subunit (ALS), or IGFBP protease activity in relation to GH release during a hypocaloric diet. The main purpose of this study was to determine free IGF-I, ALS, IGFBPs-1-4, and IGFBPs-1-3 protease activity in relation to 24-h GH release before and after a short-term very low-calorie diet (VLCD).

DESIGN

Six obese subjects before weight loss, five after an average weight loss of 36.1 kg, and five age-and sex-matched lean controls underwent a 4-day VLCD. All subjects were studied on two occasions, once during normal basic diet and again during the last day of the VLCD (1.6 MJ).

METHODS

Free IGF-I was determined by a non-competitive immunoradiometric assay.

RESULTS

Free IGF-I levels decreased in concert with increased ALS and unchanged blunted GH release after a VLCD in the obese subjects. IGFBPs-1-3 proteolytic activity was found to be unchanged by hypocaloric diet in all groups.

CONCLUSIONS

We conclude that free IGF-I decreases after a short-term hypocaloric diet in obese subjects with no concomitant change in 24-h GH release. Circulating free IGF-I per se cannot be the main mechanism of the attenuated GH release in dieting obese subjects.

摘要

目的

据报道,肥胖患者生长激素(GH)和总胰岛素样生长因子-I(IGF-I)水平降低。据推测,由胰岛素样生长因子结合蛋白(IGFBP)蛋白酶活性产生的游离(生物活性)IGF-I水平升高可能是节食肥胖受试者GH释放降低的机制。然而,关于低热量饮食期间游离IGF-I水平、酸性不稳定亚基(ALS)或IGFBP蛋白酶活性与GH释放关系的公开数据并不存在。本研究的主要目的是确定短期极低热量饮食(VLCD)前后游离IGF-I、ALS、IGFBP-1至4以及IGFBP-1至3蛋白酶活性与24小时GH释放的关系。

设计

6名减肥前的肥胖受试者、5名平均减重36.1 kg后的肥胖受试者以及5名年龄和性别匹配的瘦对照者接受了为期4天的VLCD。所有受试者均进行了两次研究,一次在正常基础饮食期间,另一次在VLCD的最后一天(1.6兆焦耳)。

方法

采用非竞争性免疫放射分析测定游离IGF-I。

结果

肥胖受试者在VLCD后,游离IGF-I水平下降,同时ALS升高,GH释放迟钝且无变化。在所有组中,低热量饮食并未改变IGFBP-1至3的蛋白水解活性。

结论

我们得出结论,肥胖受试者在短期低热量饮食后游离IGF-I降低,而24小时GH释放无相应变化。循环中的游离IGF-I本身不可能是节食肥胖受试者GH释放减弱的主要机制。

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