BACKGROUND this study set out to examine the effects of the treatment with 1,25-dihydroxyvitamin D3 (1,25D3) [150 IU/Kg (3.75 microg/Kg) one a day, for 15 days] to non-diabetic rats and in rats rendered diabetic by a single injection of streptozotocin [65 mg/kg]. RESULTS treatment with 1,25D3 to non-diabetic rats did not affect the biochemical parameters measured in the plasma and urine of these animals. Likewise, insulin receptor expression in the kidney, liver, or adipose tissue and insulin-stimulated glucose transport in adipocytes from these animals were not affected either. Treatment with 1,25D3 to streptozotocin-induced diabetic rats did not correct the hyperglycemia, hypoinsulinemia, glycosuria or ketonemia induced by the diabetes, although it partially reversed the over-expression of the insulin receptor gene in the liver and adipose tissue, without altering the normal expression of this gene in the kidney. These effects were accompanied by a normalization of the number of insulin receptors without altering receptor affinity but improving the insulin response to glucose transport in adipocytes from these diabetic animals. Moreover, a computer search in the rat insulin receptor promoter revealed the existence of two candidate vitamin D response element (VDRE) sequences located at -256/-219 bp and -653/-620 bp, the first overlapped by three and the second by four AP-2-like sites. CONCLUSION these genomic actions of 1,25D3 could represent beneficial effects associated with the amelioration of diabetes via mechanisms that possibly involve direct transcriptional activation of the rat insulin receptor gene. The candidate VDREs identified may respond to 1,25D3 via activation of the vitamin D receptor, although this remains to be investigated.

中文翻译：

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1,25-二羟基维生素 D3 对链脲佐菌素诱导的糖尿病大鼠肾脏、肝脏和脂肪组织中胰岛素受体基因表达、胰岛素受体数量和胰岛素活性的基因组作用。

背景 本研究旨在检查用 1,25-二羟基维生素 D3 (1,25D3) [150 IU/Kg (3.75 microg/Kg) 每天一次，持续 15 天] 对非糖尿病大鼠和大鼠通过单次注射链脲佐菌素 [65 mg/kg] 导致糖尿病。结果 用 1,25D3 治疗非糖尿病大鼠不影响这些动物的血浆和尿液中测量的生化参数。同样，这些动物的肾脏、肝脏或脂肪组织中的胰岛素受体表达和脂肪细胞中胰岛素刺激的葡萄糖转运也不受影响。用1,25D3治疗链脲佐菌素诱导的糖尿病大鼠不能纠正糖尿病引起的高血糖、低胰岛素血症、糖尿或酮血症，尽管它部分逆转了肝脏和脂肪组织中胰岛素受体基因的过度表达，但并未改变该基因在肾脏中的正常表达。这些作用伴随着胰岛素受体数量的正常化，而不会改变受体亲和力，但会改善这些糖尿病动物脂肪细胞中胰岛素对葡萄糖转运的反应。此外，在大鼠胰岛素受体启动子中的计算机搜索显示存在两个候选维生素 D 反应元件 (VDRE) 序列，位于 -256/-219 bp 和 -653/-620 bp，第一个重叠了三个，第二个重叠了四个类似 AP-2 的站点。结论 1、25D3 可能代表通过可能涉及大鼠胰岛素受体基因直接转录激活的机制改善糖尿病的有益作用。确定的候选 VDRE 可能通过激活维生素 D 受体对 1,25D3 产生反应，尽管这仍有待研究。