| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
This research was planned to clarify how stress responsive transcription factor ATF5 could participate in energy metabolism abnormality due to low-graded inflammation of the hypothalamus using ATF5-deffective mouse and hypothalamic immortalized cells. It was demonstrated that ATF5 was induced by endoplasmic reticulum stress detected in the hypothalamus because of obesity, and that ATF5 also mediated signals associating with ER-stress initiated mitochondrial stress from the mitochondria to the nucleus. ATF5-knockout mice demonstrated the low body-weight both in a normal meal feeding and in the high-fat meal feeding. In addition, exposure of hypothalamus cells to tributyltin, an endocrine-disrupting chemical, caused an inflammatory response leading to mitochondrial fragmentation and the repression of the appetite inhibitor α MSH. These results suggest that ATF5 could play an important role in low-graded inflammation and the obese development through the hypothalamus malfunction.
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