瘦素与绝经后骨代谢的研究进展

Advance in researches about leptin and postmenopausal bone metabolism

绝经后骨质疏松症是由于绝经所导致的骨量减少及骨组织结构变化,使骨脆性增加易于骨折,以及由骨折引起的一系列严重威胁女性健康的并发症。如何找到一种安全,有效的抗骨质疏松症药物,是目前研究的热点。瘦素(leptin)是由肥胖基因编码的一种多肽,主要由脂肪组织分泌,通过瘦素受体(leptin receptor,ObR)发挥其生物学效应。近年来研究发现瘦素除调节糖、脂代谢外,对骨代谢也具有多重调节作用。本文从人体研究、动物实验以及体外研究多个角度,就瘦素与绝经后骨代谢的关系进行了分析,以期为绝经后骨质疏松症的治疗提供新思路。

Postmenopausal osteoporosis is caused by menopause. With the decline of the estrogen,the loss of bone mineral and the deterioration of bone structure lead to the decline of bone strength and increased fracture risk. To find an effective and safe antiosteoporotic drug is one of the hot-pots in the researches about osteoporosis. Leptin is a polypeptide hormone encoded by OB gene,primarily produced by adipose tissue. Leptin combines w ith the leptin-receptor to execute its function. Leptin can regulate the metabolism of sugar and lipid. Recent studies show ed that leptin has multiple regulation functions to the metabolism of bone. This review w ill give a summary about the relationship of leptin and postmenopausal osteoporosis.