| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
A physical decline not only led to lowering quality of life, but also raised risk of all-cause mortality. Chronic kidney disease (CKD) impaired physical performance associated with muscle alteration (reno-muscular correlation) since the early stage. 5/6 nephrectomized mice (5/6Nx mice), a mild CKD model, was shown that decrease in exercise endurance associated with decrease in muscular mitochondria (mitopenia) preceded decrease in muscle strength associated with muscle atrophy. TNF-α, a representative inflammatory cytokine which was increased since the early stage of CKD, was supposed as a candidate of mitopenia. Acylated ghrelin treatment, a gastric hormone, not only increased muscle strength and muscle mass, but improved exercise endurance and mitopenia through epigenetic modification of PGC-1α gene in 5/6Nx mice. Meanwhile, IGF-1 treatment, a muscle anabolic factor, hardly improved exercise endurance and did not improve mitopenia, though increased muscle strength and muscle mass.
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