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正常人和威尔逊病患者的胰胆锌和铜分泌

Pancreaticobiliary secretion of zinc and copper in normal persons and patients with Wilson's disease.

作者信息

Lee H H, Hill G M, Sikha V K, Brewer G J, Prasad A S, Owyang C

机构信息

Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor.

出版信息

J Lab Clin Med. 1990 Sep;116(3):283-8.

PMID:2401845
Abstract

The objectives of this study were (1) to examine basal and cholecystokinin-stimulated pancreaticobiliary secretion of zinc in normal subjects with zinc-adequate and zinc-deficient diets, and (2) to investigate whether basal and stimulated secretion of zinc was abnormal in patients with Wilson's disease before and after zinc therapy. Gastroduodenal intubation was performed in six healthy subjects and five patients with Wilson's disease. After intravenous infusion of octapeptide of cholecystokinin (40 ng/kg/hr) the pancreaticobiliary secretion of zinc increased from a basal rate of 283.1 +/- 75.8 nmol/L/min to a peak of 716.6 +/- 175.3 nmol/L/min in normal subjects. Normal subjects with a zinc-deficient diet had both lower basal (66.8 +/- 15.8 nmol/L/min) and stimulated (559.5 +/- 31 nmol/L/min) pancreaticobiliary secretion of zinc than with a zinc-sufficient diet. In contrast to the markedly reduced pancreaticobiliary secretion of copper, patients with Wilson's disease not treated with zinc had normal basal (226.6 +/- 126 nmol/L/min) and stimulated (728.7 +/- 195.5 nmol/L/min) zinc secretion. These studies indicate that a considerable amount of zinc is being secreted in pancreaticobiliary fluid in healthy subjects and there was no impairment of zinc secretion in patients with Wilson's disease. Our data also indicate that pancreaticobiliary secretion of zinc is dependent on the zinc status of the subjects, suggesting that endogenous secretion of zinc may play a significant role in the homeostasis of zinc.

摘要

本研究的目的是

(1)在饮食锌充足和锌缺乏的正常受试者中,检测基础状态下以及胆囊收缩素刺激后的胰胆锌分泌;(2)调查威尔逊病患者在锌治疗前后基础状态下以及刺激后的锌分泌是否异常。对6名健康受试者和5名威尔逊病患者进行了胃十二指肠插管。静脉输注胆囊收缩素八肽(40 ng/kg/小时)后,正常受试者胰胆锌分泌从基础速率283.1±75.8 nmol/L/分钟增加到峰值716.6±175.3 nmol/L/分钟。饮食锌缺乏的正常受试者基础状态下(66.8±15.8 nmol/L/分钟)和刺激后(559.5±31 nmol/L/分钟)的胰胆锌分泌均低于饮食锌充足的受试者。与胰胆铜分泌明显减少形成对比的是,未接受锌治疗的威尔逊病患者基础状态下(226.6±126 nmol/L/分钟)和刺激后(728.7±195.5 nmol/L/分钟)的锌分泌正常。这些研究表明,健康受试者的胰胆液中分泌有相当数量的锌,威尔逊病患者的锌分泌没有受损。我们的数据还表明,胰胆锌分泌取决于受试者的锌状态,提示内源性锌分泌可能在锌的体内平衡中起重要作用。

相似文献

1
Pancreaticobiliary secretion of zinc and copper in normal persons and patients with Wilson's disease.正常人和威尔逊病患者的胰胆锌和铜分泌
J Lab Clin Med. 1990 Sep;116(3):283-8.
2
Zinc therapy increases duodenal concentrations of metallothionein and iron in Wilson's disease patients.锌疗法可提高威尔逊氏病患者十二指肠中金属硫蛋白和铁的浓度。
Am J Gastroenterol. 1999 Feb;94(2):334-8. doi: 10.1111/j.1572-0241.1999.851_w.x.
3
Treatment of Wilson's disease with zinc. VI. Initial treatment studies.锌治疗肝豆状核变性。VI. 初始治疗研究。
J Lab Clin Med. 1989 Dec;114(6):633-8.
4
Zinc treatment prevents lipid peroxidation and increases glutathione availability in Wilson's disease.锌治疗可预防威尔逊病中的脂质过氧化并增加谷胱甘肽的可用性。
J Lab Clin Med. 2003 Jun;141(6):372-7. doi: 10.1016/S0022-2143(03)00027-1.
5
Studies of cholecystokinin-stimulated biliary secretions reveal a high molecular weight copper-binding substance in normal subjects that is absent in patients with Wilson's disease.对胆囊收缩素刺激的胆汁分泌的研究显示,正常受试者体内有一种高分子量的铜结合物质,而威尔逊氏病患者体内则没有这种物质。
J Lab Clin Med. 1988 Mar;111(3):267-74.
6
[Wilson's disease].
Recenti Prog Med. 1992 May;83(5):255-61.
7
Wilson's disease: a new gene and an animal model for an old disease.威尔逊氏病:一种古老疾病的新基因与动物模型
J Investig Med. 1995 Aug;43(4):323-36.
8
Treatment of Wilson's disease with zinc: III. Prevention of reaccumulation of hepatic copper.锌治疗威尔逊病:III. 预防肝脏铜的再蓄积。
J Lab Clin Med. 1987 May;109(5):526-31.
9
A critical evaluation of copper metabolism in Indian Wilson's disease children with special reference to their phenotypes and relatives.对印度威尔逊病患儿铜代谢的批判性评估,特别参考其表型和亲属情况。
Biol Trace Elem Res. 1998 Nov;65(2):153-65. doi: 10.1007/BF02784267.
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[The onset of psychiatric disorders and Wilson's disease].[精神疾病与威尔逊氏病的发病]
Encephale. 2007 Dec;33(6):924-32. doi: 10.1016/j.encep.2006.08.009. Epub 2007 Sep 5.

引用本文的文献

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Extracellular zinc stimulates ERK-dependent activation of p21(Cip/WAF1) and inhibits proliferation of colorectal cancer cells.细胞外锌离子刺激p21(Cip/WAF1)的ERK依赖性激活并抑制结肠癌细胞的增殖。
Br J Pharmacol. 2002 Nov;137(5):597-607. doi: 10.1038/sj.bjp.0704909.
2
Effect of bile/pancreatic secretions on absorption of radioactive or stable zinc. In vivo and in vitro studies.胆汁/胰液分泌对放射性或稳定锌吸收的影响。体内和体外研究。
Biol Trace Elem Res. 1994 Aug;42(2):81-96. doi: 10.1007/BF02785381.
3
The role of the pancreas in the regulation of zinc status.
胰腺在锌状态调节中的作用。
Biol Trace Elem Res. 1994 Aug;42(2):143-9. doi: 10.1007/BF02785385.
4
Zinc: health effects and research priorities for the 1990s.锌:20世纪90年代的健康影响及研究重点
Environ Health Perspect. 1994 Jun;102 Suppl 2(Suppl 2):5-46. doi: 10.1289/ehp.941025.