Effective early prevention of osteoporosis caused by mutation of the gene coding for the aldehyde dehydrogenase 2 enzyme.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24614014
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Integrated Nutrition Science
• Research Institution: Maebashi Institute of Technology (2013-2014); The University of Tokyo (2012)
• Principal Investigator: HOSHI HIROKO 前橋工科大学, 工学部, 准教授 (50399812)
• Co-Investigator(Renkei-kenkyūsha): JIN Shigeki (60531845)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 骨粗鬆症 / 骨芽細胞 / アセトアルデヒド / 遺伝子変異 / 抗酸化物質 / アスタキサンチン

Outline of Final Research Achievements

Aldehyde dehydrogenase 2 (ALDH2) has a major role in acetaldehyde detoxification and is localized in mitochondria. About half of Japanese and East Asians have a mutant ALDH2 gene, resulting in sensitivity to alcohol. We previously showed that a dominant-negative form of Aldh2 mice showed osteoporosis caused by impaired osteoblastogenesis. In this study, we examined whether or not various nutritional factors have effects of antioxidant reagents to prevent osteoporosis in Aldh2 transgenic (ALDH2-DAL）mice and in their osteoclast cells. As the results, astaxanthin effectively inhibited the failure of osteoblasts to differentiate in a dose-dependent manner. The administration of astaxanthin to ALDH2-DAL mice led to an increasing femur bone density compared to normal-diet ALDH2-DAL mice fed for 3 months in vivo experiments. In this study, we showed that astaxanthin prevented osteoporosis caused by ALDH2 gene mutation.

Free Research Field

生化学