Abstract

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.

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