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基因导致小鼠胫骨松质骨丢失和继发性骨形成减少。在这些破坏的小鼠中，通过增强p53 mRNA的表达诱导成骨细胞凋亡，成骨细胞分化和增殖受到抑制。骨形成减少。在小鼠中，酒精摄入导致的β-脱氢酶2基因的破坏导致骨小梁丢失和骨形成减少。细胞周期阻滞通过p21 mRNA表达的增强而诱导，成骨细胞矿化受到干扰。骨形成减少。因此，我们通过细胞周期阻滞或成骨细胞凋亡证实了酒精摄入或高脂饮食诱导的骨小梁丢失的潜在机制。

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.