National Institute on Aging, Clinical Research Branch, 3001 South Hanover Street, Baltimore, Maryland 21225, USA.
J Clin Endocrinol Metab. 2011 Jun;96(6):E884-90. doi: 10.1210/jc.2010-2589. Epub 2011 Mar 9.
Preclinical studies suggested the existence of a signaling pathway connecting bone and glucose metabolisms. Supposedly leptin modulates osteocalcin bioactivity, which in turn stimulates insulin and adiponectin secretion, and β-cell proliferation.
The objective of the investigation was to study the reciprocal relationships of adiponectin, leptin, osteocalcin, insulin resistance, and insulin secretion to verify whether such relationships are consistent with a signaling pathway connecting bone homeostasis and glucose metabolism.
This was a cross-sectional analysis.
The study was conducted with community-dwelling volunteers participating in the Baltimore Longitudinal Study of Aging.
Two hundred eighty women and 300 men with complete data on fasting plasma adiponectin, leptin, and osteocalcin, oral glucose tolerance test (plasma glucose and insulin values available at t = 0, 20, and 120 min), and anthropometric measures participated in the study.
Linear regression models were used to test independent associations of adiponectin, osteocalcin, and leptin with the indices of insulin resistance and secretion. The expected reciprocal relationship between different biomarkers was verified by structural equation modeling.
In linear regression models, leptin was strongly associated with indices of both insulin resistance and secretion. Both adiponectin and osteocalcin were negatively associated with insulin resistance. Structural equation modeling revealed a direct inverse association of leptin with osteocalcin; a direct positive association of osteocalcin with adiponectin; and an inverse relationship of osteocalcin with insulin resistance and adiponectin with insulin resistance and secretion, which is cumulatively consistent with the hypothesized model.
Bone and glucose metabolisms are probably connected through a complex pathway that involves leptin, osteocalcin, and adiponectin. The clinical relevance of such a pathway for bone pathology in diabetes should be further investigated.
临床前研究表明，存在一条连接骨骼和葡萄糖代谢的信号通路。据推测，瘦素调节骨钙素的生物活性，而骨钙素反过来又刺激胰岛素和脂联素的分泌以及β细胞的增殖。
本研究旨在研究脂联素、瘦素、骨钙素、胰岛素抵抗和胰岛素分泌之间的相互关系，以验证这些关系是否与连接骨稳态和葡萄糖代谢的信号通路一致。
这是一项横断面分析。
本研究在巴尔的摩老龄化纵向研究中，对居住在社区的志愿者进行。
共有 280 名女性和 300 名男性志愿者，他们的数据完整，包括空腹血浆脂联素、瘦素和骨钙素、口服葡萄糖耐量试验（在 t = 0、20 和 120 分钟时血浆葡萄糖和胰岛素值）以及人体测量指标。
线性回归模型用于检验脂联素、骨钙素和瘦素与胰岛素抵抗和分泌指数的独立相关性。通过结构方程模型验证不同生物标志物之间预期的相互关系。
在线性回归模型中，瘦素与胰岛素抵抗和分泌的指数密切相关。脂联素和骨钙素均与胰岛素抵抗呈负相关。结构方程模型显示瘦素与骨钙素有直接的负相关关系；骨钙素与脂联素有直接的正相关关系；骨钙素与胰岛素抵抗呈负相关，脂联素与胰岛素抵抗和分泌呈负相关，这与假设模型一致。
骨骼和葡萄糖代谢可能通过涉及瘦素、骨钙素和脂联素的复杂途径相互连接。对于糖尿病中的骨病理，这种途径的临床相关性应进一步研究。
