Díaz-Corte C, Fernández-Martín J L, Barreto S, Gómez C, Fernández-Coto T, Braga S, Cannata J B
Bone and Mineral Research Unit, Instituto Reina Sofía de Investigación, Oviedo, Spain.
Nephrol Dial Transplant. 2001 Apr;16(4):742-5. doi: 10.1093/ndt/16.4.742.
Aluminium overload leads to parathyroid hormone (PTH) suppression. However, it is unclear whether a decrease in synthesis or release of the hormone is mainly involved. The aim of this study was to assess the effect of an acute administration of aluminium on PTH synthesis and release in rats with chronic renal failure and secondary hyperparathyroidism.
The study was performed using 100 adult male Wistar rats (body weight 443+/-54 g). 7/8 nephrectomy was performed and the rats were maintained on a high dietary phosphorous intake. Five weeks after surgery, the rats were randomly divided into two groups, one loaded with aluminium (AlCl3) and the other given placebo. Aluminium or placebo were administered i.p. for two consecutive days. The placebo group received saline at the same pH as the aluminium solution. After 2 weeks, serum calcium, phosphorous, creatinine, PTH, and aluminium were measured. The parathyroid glands were removed and PTH messenger RNA (mRNA) was measured by northern blot. Intact PTH was measured by IRMA (Rat PTH, Nichols Institute).
No differences in serum PTH levels were found between the two groups after 5 weeks of renal failure. At the end of the study the rats given aluminium had higher aluminium levels than the placebo group and lower PTH levels. No significant differences were found for calcium, phosphorous, renal function, or body weight. PTH mRNA expression was lower in the aluminium group than in the placebo group.
The administration of aluminium in rats with chronic renal failure resulted in reductions in serum PTH and PTH mRNA. Thus far, previous studies had demonstrated that aluminium suppressed PTH release. The present findings suggest that PTH synthesis is also reduced.
铝过载会导致甲状旁腺激素（PTH）分泌受抑制。然而，尚不清楚主要是激素合成减少还是释放减少所致。本研究旨在评估急性给予铝对慢性肾衰竭和继发性甲状旁腺功能亢进大鼠PTH合成及释放的影响。
本研究使用100只成年雄性Wistar大鼠（体重443±54 g）。进行7/8肾切除术，并让大鼠维持高磷饮食摄入。术后5周，将大鼠随机分为两组，一组给予铝（AlCl3），另一组给予安慰剂。铝或安慰剂连续两天腹腔注射。安慰剂组接受与铝溶液pH相同的生理盐水。2周后，测量血清钙、磷、肌酐、PTH和铝。切除甲状旁腺，通过Northern印迹法测量PTH信使核糖核酸（mRNA）。采用免疫放射分析法（大鼠PTH，Nichols研究所）测量完整PTH。
肾衰竭5周后，两组血清PTH水平无差异。研究结束时，给予铝的大鼠铝水平高于安慰剂组，PTH水平低于安慰剂组。钙、磷、肾功能或体重方面未发现显著差异。铝组PTH mRNA表达低于安慰剂组。
给慢性肾衰竭大鼠给予铝导致血清PTH和PTH mRNA降低。迄今为止，先前的研究已证明铝会抑制PTH释放。目前的研究结果表明PTH合成也减少。
