Sheikh M S, Ramirez A, Emmett M, Santa Ana C, Schiller L R, Fordtran J S
Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas 75246.
J Clin Invest. 1988 Jan;81(1):126-32. doi: 10.1172/JCI113283.
We measured net calcium absorption and the calcium content of the digestive glands secretions in people with widely different serum concentrations of 1,25 dihydroxy vitamin D (hereafter referred to a 1,25-D). Patients with end stage renal disease on hemodialysis served as a model of human 1,25-D deficiency; they were also studied when they had abnormally high serum 1,25-D concentrations as a result of short periods of treatment with exogenous 1,25-D. Normal subjects were studied for comparison. The amount of calcium secreted into the duodenum by the digestive glands was found to be trivial compared to the calcium content of normal or even low calcium meals; therefore, values for net and true net calcium absorption differed only slightly. There was a linear correlation between true net calcium absorption and serum 1,25-D concentration. By extrapolating the short distance to a zero value for serum 1,25-D, D-independent true net calcium absorption was estimated. By subtracting D independent from true net calcium absorption, values for D-dependent absorption were obtained. For a given level of meal calcium intake, D-dependent calcium absorption was found to be directly proportional to serum 1,25-D concentration. At any given value for serum 1,25-D, absorption via the D-dependent mechanism was approximately the same with a low (120 mg) calcium meal as it was when meal calcium intake was increased to 300 mg. We interpret this to mean that the D-dependent mechanism is saturated or nearly saturated by low calcium meals. The D-independent absorption/secretion mechanism resulted in secretion (a loss of body calcium in the feces) when intake was low (120 mg per meal) and absorption when intake was normal. All of the increment in calcium absorption that occurs when low or normal calcium meals are supplemented with extra calcium is mediated by the D-independent mechanism.
我们测量了血清1,25 - 二羟维生素D(以下简称1,25 - D)浓度差异很大的人群的净钙吸收和消化腺分泌物中的钙含量。接受血液透析的终末期肾病患者作为人体1,25 - D缺乏的模型;当他们因短期接受外源性1,25 - D治疗而血清1,25 - D浓度异常升高时,也对其进行了研究。选取正常受试者作为对照。结果发现,与正常甚至低钙膳食中的钙含量相比,消化腺分泌到十二指肠的钙量微不足道;因此,净钙吸收值和真正的净钙吸收值仅略有差异。真正的净钙吸收与血清1,25 - D浓度之间存在线性相关性。通过将血清1,25 - D浓度外推至接近零值的短距离,估算出不依赖维生素D的真正净钙吸收。用真正的净钙吸收减去不依赖维生素D的吸收,得到依赖维生素D的吸收值。对于给定水平的膳食钙摄入量,发现依赖维生素D的钙吸收与血清1,25 - D浓度成正比。在血清1,25 - D的任何给定值下,低钙(120毫克)膳食时通过依赖维生素D机制的吸收与膳食钙摄入量增加到300毫克时大致相同。我们据此推断,低钙膳食会使依赖维生素D的机制达到饱和或接近饱和。当摄入量较低(每餐120毫克)时,不依赖维生素D的吸收/分泌机制会导致钙分泌(粪便中身体钙的流失),而摄入量正常时则导致钙吸收。当低钙或正常钙膳食补充额外钙时,钙吸收增加的所有部分均由不依赖维生素D的机制介导。