Suzuki K, Ishida H, Takeshita N, Taguchi Y, Sugimoto C, Nosaka K, Seino Y
Department of Metabolism and Clinical Nutrition, Kyoto University School of Medicine, Japan.
J Diabetes Complications. 1998 May-Jun;12(3):176-80. doi: 10.1016/s1056-8727(97)00107-4.
In order to investigate the pathogenic role of bone resorption by osteoclasts in altered bone metabolism in non-insulin-dependent diabetes mellitus (NIDDM), the circulating levels of tartrate resistant acid phosphatase (TRACP) were simultaneously determined with osteocalcin, in rat models of NIDDM, i.e., genetic Wistar fatty rats and neonatally streptozotocin-induced diabetic rats (NSZ rats). In Wistar fatty rats exhibiting hyperglycemia and hyperinsulinemia, plasma TRACP was 40.0+/-0.4 U/l (mean+/-SE), significantly higher than that of 32.8+/-1.3 U/l in their lean littermates (p < 0.01). Bone length, bone strength, and weight of powdered bone in Wistar fatty rats were significantly decreased compared to control rats (p < 0.02-0.001). On the other hand, plasma TRACP in NSZ rats was 13.6+/-1.0 U/l, significantly lower than that of 31.4+/-1.2 U/l in their controls (p < 0.01). In addition, there were positive correlations between circulating TRACP and insulin levels in both NIDDM rat models (p < 0.05-0.01). Furthermore, plasma osteocalcin levels in these NIDDM models were significantly decreased than those of their corresponding controls (p < 0.001). Consequently, in Wistar fatty rats with hyperinsulinemia, it is suggested that the bone formation by osteoblasts was decreased, while the bone resorption by osteoclasts was increased. In contrast, in NSZ rats with hypoinsulinemia, both of bone formation and resorption were speculated to be decreased, indicating the decreased bone turnover. These results suggest that, although the deterioration in the osteoblastic function can be commonly observed in NIDDM animal models, the osteoclastic function is heterogeneous under NIDDM conditions.
为了研究破骨细胞骨吸收在非胰岛素依赖型糖尿病(NIDDM)骨代谢改变中的致病作用,在NIDDM大鼠模型,即遗传性Wistar肥胖大鼠和新生链脲佐菌素诱导的糖尿病大鼠(NSZ大鼠)中,同时测定了抗酒石酸酸性磷酸酶(TRACP)的循环水平和骨钙素水平。在表现出高血糖和高胰岛素血症的Wistar肥胖大鼠中,血浆TRACP为40.0±0.4 U/l(平均值±标准误),显著高于其瘦型同窝大鼠的32.8±1.3 U/l(p<0.01)。与对照大鼠相比,Wistar肥胖大鼠的骨长度、骨强度和骨粉重量显著降低(p<0.02 - 0.001)。另一方面,NSZ大鼠的血浆TRACP为13.6±1.0 U/l,显著低于其对照组的31.4±1.2 U/l(p<0.01)。此外,在两种NIDDM大鼠模型中,循环TRACP与胰岛素水平之间均存在正相关(p<0.05 - 0.01)。此外,这些NIDDM模型中的血浆骨钙素水平显著低于其相应对照组(p<0.001)。因此,在高胰岛素血症的Wistar肥胖大鼠中,提示成骨细胞的骨形成减少,而破骨细胞的骨吸收增加。相反,在低胰岛素血症的NSZ大鼠中,推测骨形成和骨吸收均减少,表明骨转换降低。这些结果表明,尽管在NIDDM动物模型中通常可观察到成骨细胞功能的恶化,但在NIDDM条件下破骨细胞功能是异质性的。