Institute of Endocrinology and Metabolism, Second Xiangya Hospital of Central South University, 139# Middle Renmin Road, Changsha, Hunan 410011, People's Republic of China.
Osteoporos Int. 2012 Apr;23(4):1425-36. doi: 10.1007/s00198-011-1697-8. Epub 2011 Jul 14.
Omentin-1 inhibited osteoblast differentiation in vitro. In co-culture systems of osteoblasts and osteoclast precursors, omentin-1 reduced osteoclast formation by stimulating osteoprotegerin (OPG) and inhibiting receptor activator for nuclear factor κB ligand (RANKL) production in osteoblasts. In vivo, adenovirus-mediated overexpression of omentin-1 suppressed bone turnover and restored bone mineral density (BMD) and bone strength in ovariectomized mice.
Omentin-1 (also intelectin-1) is a recently identified visceral adipose tissue-derived cytokine that is highly abundant in plasma. This study was undertaken to investigate the effects of omentin-1 on bone metabolism.
Osteoblast differentiation was assessed by measuring alkaline phosphatase activity, osteocalcin production and matrix mineralization. OPG and RANKL protein expression and secretion in osteoblasts were detected by Western blot and ELISA, respectively. The effect of recombinant omentin-1 on osteoclast formation was examined in co-culture systems of osteoblasts and osteoclast precursors. The effects of intravenous administration of adenoviral-delivered omentin-1 on bone mass, bone strength, and bone turnover were also examined in ovariectomized mice.
In vitro, omentin-1 inhibited osteoblast differentiation, while it had no direct effect on osteoclast differentiation; it also reduced osteoclast formation in the co-culture systems through stimulating OPG and inhibiting RANKL production in osteoblasts. In vivo, adenovirus-mediated overexpression of omentin-1 partially restored BMD and bone strength in ovariectomized mice, accompanied by decreased levels of plasma osteocalcin and tartrate-resistant acid phosphatase-5b and lower serum RANKL/OPG ratios.
The present study suggests that omentin-1 ameliorates bone loss induced by estrogen deficiency via downregulating the RANKL/OPG ratio.
网膜素-1 可抑制体外成骨细胞分化。在成骨细胞与破骨细胞前体细胞的共培养体系中，网膜素-1 通过刺激骨保护素（OPG）和抑制核因子κB 受体激活剂配体（RANKL）在成骨细胞中的产生，减少破骨细胞的形成。在体内，腺病毒介导的网膜素-1 过表达抑制了去卵巢小鼠的骨转换，并恢复了骨密度（BMD）和骨强度。
网膜素-1（也称为intelectin-1）是一种最近发现的内脏脂肪组织来源的细胞因子，在血浆中含量丰富。本研究旨在探讨网膜素-1 对骨代谢的影响。
通过测量碱性磷酸酶活性、骨钙素产生和基质矿化来评估成骨细胞分化。通过 Western blot 和 ELISA 分别检测成骨细胞中 OPG 和 RANKL 蛋白的表达和分泌。在成骨细胞与破骨细胞前体细胞的共培养体系中，检测重组网膜素-1 对破骨细胞形成的影响。还在去卵巢小鼠中检测了静脉注射腺病毒递送的网膜素-1 对骨量、骨强度和骨转换的影响。
在体外，网膜素-1 抑制成骨细胞分化，而对破骨细胞分化没有直接影响；它还通过刺激成骨细胞中 OPG 的产生和抑制 RANKL 的产生，减少共培养体系中的破骨细胞形成。在体内，腺病毒介导的网膜素-1 过表达部分恢复了去卵巢小鼠的 BMD 和骨强度，同时降低了血浆骨钙素和抗酒石酸酸性磷酸酶-5b 的水平，以及血清 RANKL/OPG 比值。
本研究表明，网膜素-1 通过下调 RANKL/OPG 比值改善了雌激素缺乏引起的骨丢失。
