| Budget Amount *help |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2015: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Outline of Final Research Achievements |
Osteoporosis is a skeletal disease characterized by an increased susceptibility to fractures. Evidence from genetic analyses indicates that pathogenesis of osteoporosis is genetically controlled. We show that the SLC25A32, the mitochondrial inner membrane folate transporter, gene polymorphism could be a risk factor for lower folate concentration and future fracture. Moreover, we have identified single-nucleotide polymorphisms (SNPs) that are associated with the development of sarcopenia, which is characterized by a loss of lean body mass, and obesity, which is characterized by high fat mass by genome-wide association studies (GWAS). Here, we have shown that GWAS revealed a functional SNP in the 5'-flanking region of PRDM16 gene associated with lean body mass. We also found that genetic analyses in human and knock out mouse models revealed the importance of SLC25A24/Slc25a24 in the regulation of body fat mass and adipogenesis.
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