| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
We examined the gene expressions of visceral adipose tissue related to inflammation and endoplasmic reticulum (ER) stress response in Japanese subjects with morbid obesity. The expressions of TNF-a increased 4.0fold(p=0.0082), CHOP 1.7 fold (p=0.0034), compared to non-obese subjects. These results showed thatinflammation and ER stress response were aggravated in adipose tissue with obesity as reported in animal experiment.
Obesity represents chronic inflammatory states promoted by pro-inflammatory M1-macrophage infiltration into adipose tissue, thereby inducing insulin resistance. Obesity enhances ER stress with CHOP upregulation in adipocytes. CHOP deficiency prevents obesity induced insulin resistancewith M2 macrophage predomination and Th2 cytokine upregulation in WAT. Whereas ER stress suppresses Th2 cytokine expression in cultured adipocytes, CHOP knockdown inhibits this downregulation.This molecular mechanism may link adipose ER stress with systemic insulin resistance.
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