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胰岛素刺激试验后尿铬排泄不能作为铬营养状况的生物标志物。

Urinary chromium excretion in response to an insulin challenge is not a biomarker for chromium status.

机构信息

Department of Chemistry, The University of Alabama, Tuscaloosa, AL 35487-0336, USA.

出版信息

Biol Trace Elem Res. 2013 Apr;152(1):57-65. doi: 10.1007/s12011-012-9594-3. Epub 2013 Jan 8.

Abstract

Over 50 years ago, chromium (Cr) was proposed to be an essential trace element; however, recent studies indicate that this status should be removed as the effects of Cr supplementation appear to be pharmacological rather than nutritional. The pharmacological basis for Cr's effects can explain the inability of investigators to discover a biomarker for Cr status. One potential biomarker has not been examined to date. Cr is known to be mobilized in the body in response to insulin (or insulin release in response to a glucose challenge), resulting in an increase in urinary Cr excretion. The magnitude of increase in urinary Cr loss as a function of dietary Cr intake was tested as a potential biomarker for Cr. Zucker lean rats housed in carefully controlled metal-free conditions were provided a series of purified diets containing variable Cr contents (from 16 μg/kg diet to 2,000 μg/kg) for 23 weeks. The 16 μg/kg diet contained less Cr than any diet examined to date. Urine samples were collected before and after insulin and glucose challenges (0, 2, 6, and 12 h postinjection). Urinary Cr levels were analyzed by the standard method of addition using graphite furnace atomic absorption. The rate of urinary Cr loss after a glucose or insulin challenge was found to not be dependent on the Cr content of the rats' diets. Blood iron levels of the rats were also measured to determine if the addition of Cr to the diet altered iron status. The Cr content of the diet was found to have no affect on blood iron levels. Overall, the study demonstrated that insulin-stimulated urinary Cr excretion cannot be used as a biomarker for Cr status.

摘要

50 多年前,铬(Cr)被提议为一种必需的微量元素;然而,最近的研究表明,这种地位应该被取消,因为 Cr 补充的效果似乎是药理学的,而不是营养性的。Cr 效应的药理学基础可以解释研究人员无法发现 Cr 状态的生物标志物的原因。迄今为止,尚未检查一种潜在的生物标志物。已知 Cr 会响应胰岛素(或葡萄糖挑战时胰岛素的释放)在体内动员,导致尿 Cr 排泄增加。作为 Cr 摄入量的函数,尿 Cr 损失增加的幅度被测试为 Cr 的潜在生物标志物。在精心控制的无金属条件下饲养的 Zucker 瘦鼠被提供了一系列含有不同 Cr 含量的纯化饮食(从 16 μg/kg 饮食到 2000 μg/kg),为期 23 周。16 μg/kg 的饮食中 Cr 的含量低于迄今为止检查过的任何饮食。在胰岛素和葡萄糖挑战前和后(注射后 0、2、6 和 12 小时)收集尿液样本。使用石墨炉原子吸收法通过标准的添加法分析尿 Cr 水平。发现葡萄糖或胰岛素挑战后尿 Cr 损失的速度不依赖于大鼠饮食中的 Cr 含量。还测量了大鼠的血液铁水平,以确定饮食中添加 Cr 是否改变了铁的状态。发现饮食中的 Cr 含量对血液铁水平没有影响。总的来说,该研究表明,胰岛素刺激的尿 Cr 排泄不能用作 Cr 状态的生物标志物。

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