Effects of nutrition and alcohol consumption on bone loss.
Effects of nutrition and alcohol consumption on bone loss.
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DOI：
10.1007/s11914-011-0049-0
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发表时间：
2011-06
影响因子：
4.3
通讯作者：
Chen, Jin-Ran
中科院分区：
文献类型：
--
作者：
Ronis, Martin J J;Mercer, Kelly;Chen, Jin-Ran
众所周知，过量食用高脂肪饮食会导致肥胖。然而，肥胖对骨骼发育、成熟和重塑的影响一直存在争议。新的研究表明，肥胖和高脂肪喂养后，生长中的骨骼对机械负荷的反应受损，小梁骨量减少。至少在某种程度上，这是脂肪酸抑制 Wnt 信号传导和激活间充质干细胞中 PPARγ 通路的直接结果。由于氧化应激，长期饮酒后也会对 Wnt 和 PPARγ 信号传导产生类似的影响，并导致骨形成受到抑制，并伴有骨髓肥胖增加。由于骨细胞中 NADPH 氧化酶活性增加，酒精诱导的氧化应激也会导致 RANKL-RANK 信号增强，从而增加破骨细胞生成。相反，食用水果和豆类（例如蓝莓和大豆）会增加骨骼形成。新数据表明，Wnt 和 BMP 信号通路是源自饮食的骨合成代谢因子的分子靶标。
It is well established that excessive consumption of high fat diets results in obesity. However, the consequences of obesity of skeletal development, maturation and remodeling have been the subject of controversy. New studies suggest that the response of the growing skeleton to mechanical loading is impaired and trabecular bone mass is decreased in obesity and after high fat feeding. At least in part, this occurs as a direct result of inhibited Wnt signaling and activation of PPARγ pathways in mesenchymal stem cells by fatty acids. Similar effects on Wnt and PPARγ signaling occur after chronic alcohol consumption as the result of oxidative stress and result in inhibited bone formation accompanied by increased bone marrow adiposity. Alcohol-induced oxidative stress as the result of increased NADPH-oxidase activity in bone cells also results in enhanced RANKL-RANK signaling to increase osteoclastogenesis. In contrast, consumption of fruits and legumes such as blueberries and soy increase bone formation. New data suggest that Wnt and BMP signaling pathways are the molecular targets for bone anabolic factors derived from the diet.