| Budget Amount *help |
¥41,210,000 (Direct Cost: ¥31,700,000、Indirect Cost: ¥9,510,000)
Fiscal Year 2017: ¥10,010,000 (Direct Cost: ¥7,700,000、Indirect Cost: ¥2,310,000)
Fiscal Year 2016: ¥10,010,000 (Direct Cost: ¥7,700,000、Indirect Cost: ¥2,310,000)
Fiscal Year 2015: ¥10,010,000 (Direct Cost: ¥7,700,000、Indirect Cost: ¥2,310,000)
Fiscal Year 2014: ¥11,180,000 (Direct Cost: ¥8,600,000、Indirect Cost: ¥2,580,000)
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| Outline of Final Research Achievements |
We investigated autophagic change in the liver and the effect on liver apoptosis and lipid accumulation in NAFLD model. In liver cell lines, palmitic acid (PA) treatment suppressed autophagy with increase of Rubicon. Rubicon blockade attenuated autophagy impairment and reduced palmitate-induced apoptosis and lipid accumulation. The Rubicon increase by PA was caused by suppression of Rubicon degradation. Rubicon was also up-regulated in association with autophagy impairment in livers of mice fed a high-fat diet (HFD). Hepatocyte-specific Rubicon knockout mice showed amelioration of liver steatosis and injury as well as attenuation of autophagy impairment for four months HFD feeding. In humans, liver tissues obtained from patients with NAFLD expressed significantly higher levels of Rubicon than those without steatosis. Rubicon might be a new therapeutic target for NAFLD progression.
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