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锌缺乏会降低大鼠脂肪细胞中瘦素基因的表达及瘦素分泌。

Zinc deficiency reduces leptin gene expression and leptin secretion in rat adipocytes.

作者信息

Ott E S, Shay N F

机构信息

University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.

出版信息

Exp Biol Med (Maywood). 2001 Oct;226(9):841-6. doi: 10.1177/153537020122600906.

Abstract

The present study was conducted to measure ob mRNA abundance in the zinc-deficient (ZD) rats and the secretion of leptin from adipose tissue obtained from ZD, zinc-adequate (ZA), and pair-fed (PF) rats. It was found that ob mRNA abundance was greatest (P < 0.05) in adipose tissue obtained from ZA and PF rats. Ob mRNA abundance was similar in PF and ZD rats. To study leptin secretion from adipose tissue in a cell culture model, a method was developed to use excised epididymal adipose tissue from ZD, ZA, and PF rats. Tissue was incubated in Opti-modified Eagle's medium (MEM) cell culture medium in which concentrations of zinc and insulin were manipulated. It was observed that leptin secretion was higher (P < 0.05) in adipose tissue obtained from ZA than ZD and PF rats. Secretion of leptin was higher in adipose tissue of PF than ZD rats (P < 0.05). Surprisingly, media zinc content in this ex vivo model tended to suppress secretion of leptin. This suppression seems to be zinc specific and might be caused by the sequestration of insulin in the culture medium. Our results indicate that the reduction in serum leptin observed in ZD rats is likely caused by not only a reduction in body fat, but also by a decrease in leptin synthesis and secretion per gram of adipose tissue. Taking these results into account along with a prior study (1), it is possible that even a marginal zinc deficiency could affect leptin secretion and serum leptin concentrations. Impaired leptin secretion caused by zinc deficiency might be one factor contributing to hypogonadism observed in zinc deficiency.

摘要

本研究旨在测定锌缺乏(ZD)大鼠体内ob mRNA丰度,以及从ZD大鼠、锌充足(ZA)大鼠和配对喂养(PF)大鼠获取的脂肪组织中瘦素的分泌情况。结果发现,从ZA大鼠和PF大鼠获取的脂肪组织中ob mRNA丰度最高(P<0.05)。PF大鼠和ZD大鼠的ob mRNA丰度相似。为了在细胞培养模型中研究脂肪组织的瘦素分泌,开发了一种方法,使用从ZD大鼠、ZA大鼠和PF大鼠切除的附睾脂肪组织。将组织在Opti-改良伊格尔培养基(MEM)细胞培养基中孵育,其中锌和胰岛素的浓度受到控制。观察到,从ZA大鼠获取的脂肪组织中瘦素分泌高于ZD大鼠和PF大鼠(P<0.05)。PF大鼠脂肪组织中的瘦素分泌高于ZD大鼠(P<0.05)。令人惊讶的是,在这个体外模型中,培养基中的锌含量倾向于抑制瘦素的分泌。这种抑制似乎是锌特异性的,可能是由培养基中胰岛素的螯合作用引起的。我们的结果表明,ZD大鼠血清瘦素的降低可能不仅是由于体脂减少,还由于每克脂肪组织中瘦素合成和分泌的减少。将这些结果与之前的一项研究(1)结合起来考虑,即使是边缘性锌缺乏也可能影响瘦素分泌和血清瘦素浓度。锌缺乏导致的瘦素分泌受损可能是锌缺乏时观察到的性腺功能减退的一个促成因素。

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