Influences of the leptin on jaw bone metabolism in pediatric diabetes

在日本，与肥胖相关的疾病出现在轻度到中度肥胖的儿童和青少年中。然而，超重和高胆固醇水平与骨脆性之间的关系尚不清楚。此外，血清瘦素、脂联素与生长期骨量的关系尚不清楚。这项研究的目的是确定饮食诱导的肥胖是否会影响骨组织数量和骨强度，或者两者的组合。此外，我们还评估了骨矿物质参数与瘦素和脂联素之间的可能相关性。高脂饮食诱导的肥胖导致了生长期小鼠胫骨的脆性。在小梁骨中，随着饮食诱导肥胖小鼠皮质骨密度的下降，脂肪细胞数量的增加导致骨密度下降。在所有小鼠中，瘦素与骨小梁密度和骨横截面积呈显著负相关。而皮质骨密度与骨横截面积呈显著正相关。这些结果表明，血清瘦素和脂联素水平与骨小梁和皮质骨密度相关，但这两个部位的影响在生长中的小鼠胫骨中受到不同的调节。

In Japan, obesity-associated disorders arise in mildly to moderately obese children and adolescents. However, relationship between overweight with high cholesterol level and bone fragility are unknown. Furthermore, relationship of serum leptin and adiponectin and bone mass during growing phase are still unclear. The propose of this study is to determine whether diet-induced obesity affects bone tissue quantity and bone strength, or combinations of the two. In addition, we evaluated the possible correlations between bone mineral parameters and leptin and adiponectin. A high-fat diet-induced obesity induced bone fragility of the tibia in the growing mice. In trabecular bone, bone density was decreased by an increase in the number of adipocytes, following a decrease in the cortical bone density in the diet-induced obesity mice. In overall mice, there was a significant inverse correlation between leptin and trabecular bone density and bone cross-sectional area. However, there is a significant positive correlation between cortical bone density and bone cross-sectional area. These results suggested that serum leptin and adiponectin levels were correlated with trabecular and cortical bone density, but these effects in these two sites is regulated differently in the growing mice tibia.