Insulin expression in rats exposed to cadmium.

Li-Jian Lei, Tai-Yi Jin, Yuan-Fen Zhou
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Abstract

Objectives: To investigate the effects of cadmium exposure on insulin expression in rats.

Methods: Eighteen adult SD rats were administered cadmium subcutaneously (0.5, 1.0, and 2.0 mg/kg x bw). The effects on endocrine of pancreas were assessed. The levels of cadmium and zinc in pancreas, blood and urine glucose, serum insulin and urine NAG (N-acyetyl-beta-glucosaminidase) were determined. The gene expressions of metallothionein (MT) and insulin were also measured, and the oral glucose tolerance tests (OGTT) were carried out.

Results: The contents of cadmium in pancreas in cadmium-treated rats were higher than that in the control group, which was associated with slight increase of zinc in pancreas. Cadmium-exposed rats (1.0 and 2.0 mg/kg x bw) demonstrated a marked glucose intolerance. But the levels of serum insulin did not change significantly after cadmium administration, and the UNAG had no change in Cd-treated group. The gene expression of insulin decreased in 1.0 and 2.0 mg/kg x bw cadmium-exposed groups, compared with the control group. The expression of MT-I was higher in the groups exposed to 1.0 and 2.0 mg/kg x bw cadmium while the expression of MT-II was higher in the group exposed to 2.0 mg/kg x bw cadmium.

Conclusions: Cadmium may be accumulated in the pancreas, resulting in the change of the expression of insulin, MT-I and MT-II genes. Cadmium can influence the biosynthesis of insulin, but does not induce the release of insulin. The dysfunction of pancreas occurs earlier than that of kidney after administration of cadmium.

镉暴露大鼠胰岛素表达。
目的:探讨镉暴露对大鼠胰岛素表达的影响。方法:18只成年SD大鼠皮下注射镉(0.5、1.0、2.0 mg/kg × bw)。评价对胰腺内分泌的影响。测定胰腺中镉、锌、血、尿葡萄糖、血清胰岛素和尿NAG (n -乙酰- β -氨基葡萄糖酶)水平。同时检测金属硫蛋白(MT)和胰岛素基因表达,并进行口服糖耐量试验(OGTT)。结果:镉处理大鼠胰腺中镉含量高于对照组,与胰腺中锌含量轻微升高有关。镉暴露大鼠(1.0和2.0 mg/kg x bw)表现出明显的葡萄糖耐受不良。镉处理组血清胰岛素水平无明显变化,UNAG无明显变化。与对照组相比,1.0和2.0 mg/kg × bw镉暴露组胰岛素基因表达降低。1.0和2.0 mg/kg × bw镉处理组MT-I表达量较高,2.0 mg/kg × bw镉处理组MT-II表达量较高。结论:镉可能在胰腺中蓄积,导致胰岛素、MT-I和MT-II基因表达的改变。镉可以影响胰岛素的生物合成,但不诱导胰岛素的释放。镉中毒后胰腺功能障碍的发生早于肾脏功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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