Heath H, Lambert P W, Service F J, Arnaud S B
J Clin Endocrinol Metab. 1979 Sep;49(3):462-6. doi: 10.1210/jcem-49-3-462.
Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.
实验性糖尿病大鼠血清1,25 - 二羟维生素D水平低、肠道钙吸收不良、继发性甲状旁腺功能亢进及骨质流失。为检验与糖尿病大鼠相似的异常情况可能解释人类糖尿病性骨质减少这一假说，我们研究了40名18至75岁健康对照者及82名糖尿病患者的钙代谢情况[47名未治疗者：空腹血糖（均值±标准误），267±8mg/dl；19名接受治疗但血糖仍高者：血糖305±24mg/dl；16名接受治疗且病情控制较好者：血糖146±8mg/dl]。三组糖尿病患者的血清总钙、离子钙、免疫反应性甲状旁腺激素（阿诺德法，使用GP - 1M和CH - 12M抗血清）、25 - 羟维生素D（哈达德法）及1,25 - 二羟维生素D（兰伯特法）浓度均正常，且与对照组的值无显著差异。我们采用双同位素法（100mg钙载体；正常范围40 - 80%）测定了11名对照者及13名未治疗、血糖未控制的糖尿病患者（平均血浆葡萄糖水平285±17mg/dl）的肠道钙吸收情况。对照组的钙吸收为60±3%，糖尿病患者为56±3%（无显著差异）。我们发现，无论治疗状态如何，需要胰岛素治疗的青少年及成人起病型糖尿病成年患者均无钙代谢紊乱。实验性糖尿病大鼠模型似乎无助于确定成人人类糖尿病性骨质减少的发病机制。
