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静脉注射胰岛素推注对健康受试者尿钙和草酸排泄的影响。

Effects of i.v. insulin bolus on urinary calcium and oxalate excretion in healthy subjects.

作者信息

Nguyen N U, Dumoulin G, Henriet M T, Regnard J

机构信息

Explorations Fonctionelles Rénales Métaboliques et Endocriniennes et Laboratoire de Physiologie, CHU de Besançon, France.

出版信息

Horm Metab Res. 1998 Apr;30(4):222-6. doi: 10.1055/s-2007-978870.

Abstract

Oral glucose load increases urinary excretion of calcium (Ca) and oxalate. Although this increase in calciuria is commonly ascribed to insulin, the role of glucose on Ca excretion remains unclear. In order to assess the role of glucose changes on calciuric response to insulin and oxalate excretion, hypoglycemia induced by insulin (hypo) and hyperglycemia induced by oral glucose load (hyper) were studied in 7 healthy subjects on two separate days. As expected, glycemia dropped in hypo (-70%, p<0.001) and increased in hyper (+67%, p<0.001). Calciuria increased on the two days,+205%, p<0.001 (hypo) vs + 43%, p < 0.05 (hyper) as a result of both a rise in calcium filtered load (FCa) and a decrease in tubular reabsorption of calcium (TRCa). While the increase in FCa was similar in the two situations, the higher increased calciuria in hypo (p<0.01) was linked to a deeper decrease in TRCa, - 2.1 % (hypo) vs - 1.4% (hyper), p < 0.01. Although the estimated amounts of insulin were similar in the two situations, the insulin kinetics were different. Thus, after insulin injection, the putative role of the high initial insulin spike in triggering the increase in calciuria cannot be ruled out. The deeper decrease in TRCa (hypo) was also likely due to both hypoglycemia and changes in counter-regulation hormones. In conclusion, calciuria increased after either hypo or hyperglycemia and the higher increase in calciuria observed in hypo was subsequent to a deeper decrease in tubular Ca reabsorption. Oxaluria did not change in hypo, while it increased in hyper.

摘要

口服葡萄糖负荷会增加尿钙和草酸的排泄。虽然这种尿钙增加通常归因于胰岛素,但葡萄糖对钙排泄的作用仍不清楚。为了评估葡萄糖变化对胰岛素所致尿钙反应和草酸排泄的作用,在7名健康受试者的两个不同日子里,分别研究了胰岛素诱导的低血糖(低血糖)和口服葡萄糖负荷诱导的高血糖(高血糖)。正如预期的那样,低血糖时血糖下降(-70%,p<0.001),高血糖时血糖升高(+67%,p<0.001)。由于钙滤过负荷(FCa)增加和肾小管钙重吸收(TRCa)减少,两天内尿钙均增加,低血糖时增加205%,p<0.001,高血糖时增加43%,p<0.05。虽然两种情况下FCa的增加相似,但低血糖时尿钙增加更高(p<0.01)与TRCa更深程度的下降有关,低血糖时为-2.1%,高血糖时为-1.4%,p<0.01。虽然两种情况下估计的胰岛素量相似,但胰岛素动力学不同。因此,胰岛素注射后,不能排除高初始胰岛素峰值在引发尿钙增加中的假定作用。TRCa更深程度的下降(低血糖)也可能是由于低血糖和反调节激素的变化。总之,低血糖或高血糖后尿钙均增加,低血糖时观察到的尿钙更高增加是由于肾小管钙重吸收更深程度的下降所致。低血糖时草酸尿没有变化,而高血糖时草酸尿增加。

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