Hampson G, Evans C, Petitt R J, Evans W D, Woodhead S J, Peters J R, Ralston S H
Department of Chemical Pathology, St Thomas' Hospital, London, UK.
Diabetologia. 1998 Nov;41(11):1314-20. doi: 10.1007/s001250051071.
Osteopenia is a recognised complication of diabetes mellitus which could be due to abnormal bone turnover or disturbances in the calcium/parathyroid hormone/vitamin D axis or both. Genetic factors also play an important part in determining bone mass although this has not been studied in diabetes. Recently a polymorphism of the collagen type 1 alpha 1 (COL1A1) gene has been shown to be associated with low bone mass in British women. To identify subjects with diabetes who may be at risk of developing osteoporosis and fractures, we analysed bone mineral density in relation to the biochemical markers of bone turnover, calcium homeostasis and the COL1A1 genotype in a group of premenopausal women with Type I (insulin-dependent) diabetes mellitus (n = 31), Type II (non-insulin dependent) diabetes mellitus (n = 21) and control subjects (n = 20). Bone mineral density was lower at the femoral neck in the subjects with Type I diabetes (p = 0.08) as were serum 25-hydroxyvitamin D compared with control subjects (p = 0.023) and this was negatively correlated with serum collagen type 1 C-terminal propeptide (r = -0.56, p < 0.001). Bone mineral density in Type II diabetes was not different from control subjects, after correction for body mass index. Bone resorption was, however, raised in the Type II diabetic subjects as reflected by the higher urinary deoxypyridinoline values (p = 0.016) and lower collagen type 1 C-terminal propeptide:deoxypyridinoline ratio (p = 0.04). In the whole group studied, subjects with the COL1A1 's' genotype had lower bone mineral density at the femoral neck (p = 0.01) which was partly attributable to a lower body mass index. Following multiple regression analysis body mass index and collagen type 1 C-terminal propeptide concentrations remained determinants of bone mass at all three sites, whereas genotype appeared to be a predictor of bone mass at the femoral neck only. We conclude that measurement of these variables could prove useful in firstly identifying those diabetic women at risk of osteoporosis and secondly guiding therapeutic intervention.
骨质减少是糖尿病公认的并发症，其可能归因于骨转换异常或钙/甲状旁腺激素/维生素D轴紊乱，或两者皆有。遗传因素在决定骨量方面也起着重要作用，尽管糖尿病患者尚未对此进行研究。最近，在英国女性中发现1型胶原蛋白α1（COL1A1）基因的多态性与低骨量有关。为了确定可能有患骨质疏松症和骨折风险的糖尿病患者，我们分析了一组绝经前1型（胰岛素依赖型）糖尿病患者（n = 31）、2型（非胰岛素依赖型）糖尿病患者（n = 21）和对照受试者（n = 20）的骨矿物质密度与骨转换、钙稳态生化标志物以及COL1A1基因型的关系。1型糖尿病患者的股骨颈骨矿物质密度较低（p = 0.08），血清25-羟维生素D水平也低于对照受试者（p = 0.023），且与血清1型胶原蛋白C末端前肽呈负相关（r = -0.56，p < 0.001）。校正体重指数后，2型糖尿病患者的骨矿物质密度与对照受试者无差异。然而，2型糖尿病患者的骨吸收增加，尿脱氧吡啶啉值较高（p = 0.016），1型胶原蛋白C末端前肽与脱氧吡啶啉比值较低（p = 0.04）。在整个研究组中，具有COL1A1“s”基因型的受试者股骨颈骨矿物质密度较低（p = 0.01），这部分归因于较低的体重指数。多元回归分析后发现，体重指数和1型胶原蛋白C末端前肽浓度仍是所有三个部位骨量的决定因素，而基因型似乎仅是股骨颈骨量的预测指标。我们得出结论，测量这些变量可能有助于首先识别有骨质疏松症风险的糖尿病女性，其次指导治疗干预。
