Investigation of disorders of interaction between bone and bone marrow after intake of alcohol and fat

高脂饮食破坏载脂蛋白E基因导致小鼠胫骨次级松质骨的骨小梁丢失和骨形成减少。在这些被破坏的小鼠中，成骨细胞通过增强P53基因的表达而诱导细胞凋亡，成骨细胞的分化和增殖受到抑制。骨形成减少。酒精摄入破坏乙醛脱氢酶2基因，导致小鼠骨小梁丢失和骨形成减少。P21mRNA表达增强导致细胞周期停滞，成骨细胞矿化受到干扰。骨形成减少。因此，我们通过细胞周期停滞或成骨细胞的凋亡来阐明酒精摄入或高脂饮食导致骨小梁丢失的机制。

Disruption of Apo E gene with high fat diet resulted in trabecular bone loss and reduced bone formation at the secondary spongiosa of the tibia in mice. In these disrupted mice, apoptosis was induced in osteoblasts through enhanced expression of p53 mRNA and osteoblastic differentiation and proliferation were suppressed. Bone formation was decreased. Disruption of aldehyde-dehydrogenase 2 gene with alcohol intake resulted in trabecular bone loss and reduced bone formation in mice. Cell cycle arrest was induced through enhanced expression of p21 mRNA and osteoblastic mineralization was disturbed. Bone formation was decreased. Thus, we demonstrated the mechanism underlying trabecular bone loss induced by alcohol intake or high fat diet through cell cycle arrest or apoptosis of osteoblasts.