| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Obesity and insulin resistance in the mother might play a direct role in the transmission of an obesogenic and diabetogenic trait from generation to generation, but the role of genes and a shared environment are not completely understood.
We observed that a high fat diet induced obesity in pregnant mice resulted in hypertension, proteinuria, and macrosomia with insulin resistance and abnormal adipocytokine levels and that the exposure to a high fat diet in utero might lead to a metabolic syndrome-like phenomenon through epigenetic modifications of the genes encoding adipocytokines, adiponectin and leptin in the offspring. We also demonstrated that activation of constitutive androstane receptor ameliorated the glucose metabolism in both mothers and adult offspring. Epigenetic changes of adipocytokine genes might play important roles in the origin of metabolic syndrome in adulthood of offspring and constitutive androstane receptor might be a potential therapeutic target.
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