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KAKEN_17K19668seika.pdf
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Download
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:974.8 KB
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:Oct 31, 2019 |
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Total downloads since Oct 31, 2019 : 901
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肥満、糖尿病関連遺伝子レプチンと炎症性腸疾患の関連性の検討
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ヒマン、トウニョウビョウ カンレン イデンシ レプチン ト エンショウセイ チョウ シッカン ノ カンレンセイ ノ ケントウ
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Himan, tōnyōbyō kanren idenshi repuchin to enshōsei chō shikkan no kanrensei no kentō
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Analyse of leptin signal in inflammatory bowel disease
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筋野, 智久
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スジノ, トモヒサ
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Sujino, Tomohisa
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慶應義塾大学・医学部 (信濃町)・特任講師
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Research team head
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科研費研究者番号 : 40464862
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2019
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科学研究費補助金研究成果報告書
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2018
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レプチンはホルモンの一種であり、食事摂取後に脳内、筋肉、褐色脂肪細胞に働き、インスリン感受性、及び血糖の上昇抑制に役割を果たしていることが知られている。近年レプチンの受容体がT細胞上にもあることが発見され、様々な腸炎モデルにてレプチン欠損では腸炎が誘導されにくいことが示されている。レプチンシグナルの下流シグナルはSTAT3経路、mTOR/Akt経路があり、前者はTh17細胞誘導に必須であることが示されている。腸管上皮内の炎症抑制Ｔ細胞誘導においてレプチン下流のmTOR/AKtシグナルが重要であることを見出した。
Leptin is a type of hormone and is known to act on brain, muscle and brown fat cells in the brain after eating, and play a role in insulin sensitivity and suppression of blood sugar elevation. In recent years, it has been discovered that leptin receptors are also present on T cells, and it has been shown that leptin deficiency is less likely to be induced in various enteritis models. The downstream signal of leptin signal is STAT3 pathway, mTOR / Akt pathway, and the former paper has been shown to be essential for Th17 cell induction. We found that the mTOR / AKt signal downstream of leptin is important in the induction of anti-inflammatory CD4CD8aa T cells in the intestinal epithelium.
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研究種目 : 挑戦的研究(萌芽)
研究期間 : 2017～2018
課題番号 : 17K19668
研究分野 : 消化器内科
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