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KAKEN_23580139seika.pdf
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| Title |
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メタボリック症候群新規治療法を目指したβ酸化調節鍵因子ACC2の発現制御機構解明
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メタボリック ショウコウグン シンキ チリョウホウ オ メザシタ β サンカ チョウセツ カギ インシ ACC2 ノ ハツゲン セイギョ キコウ カイメイ
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Metaborikku shokogun shinki chiryoho o mezashita β sanka chosetsu kagi inshi ACC2 no hatsugen seigyo kiko kaimei
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The expression of beta-oxidation adjustment key factor ACC2 elucidation which aimed at the metabolic syndrome new therapy
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渡辺, 光博
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ワタナベ, ミツヒロ
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Watanabe, Mitsuhiro
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慶應義塾大学・政策・メディア研究科・教授
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Research team head
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科研費研究者番号 : 10450842
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森本, 耕吉
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モリモト, コウキチ
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Morimoto, Kokichi
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慶應義塾大学 医学部 助教
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Research team member
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科研費研究者番号 : 10468506
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2014
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科学研究費補助金研究成果報告書
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2013
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| Abstract |
本研究では、メタボリックシンドローム治療標的としてAcetyl-CoA Carboxylase 2(ACC2)に着目した。ACC2はエネルギー代謝改善につながる治療標的たりうるが、我々は胆汁酸投与によるマウス肝ACC2遺伝子発現低下を見出しており、これを踏まえACC2転写制御機構解明を目指した。マウスACC2遺伝子には2つの転写開始点があり、本研究で各調節領域を検討、また各mRNAの諸条件下での発現変化を検討した。その結果、2種類のmRNAは異なる発現様式を示し、特に3'側のmRNA発現に関与する機序が肝内エネルギー代謝改善の治療標的となる可能性が示された。
We propose that Acetyl-CoA Carboxylase 2 (ACC2) is an attractive therapeutic target of metabolic syndrome, and we analyzed the mechanisms implied in the regulation of ACC2 gene expression to develop a brand-new therapeutic approach of metabolic syndrome. Prior to this study, we had found that hepatic ACC2 expression was repressed by cholic acid administration in mice. We had also found that murine ACC2 gene had two different transcription initiation sites with two different transcriptional regulatory regions. In this study, we analyzed the transcriptional regulatory regions by cloning. We also investigated the alterations of the expressions of the ACC2 mRNA subtypes under special conditions such as high-fat feeding, fasting, and refeeding. According to our result, the regulatory mechanisms participated in the expression of the 3-side ACC2 mRNA seemed to become an therapeutic target to improve hepatic energy homeostasis.
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研究種目 : 基盤研究(C)
研究期間 : 2011～2013
課題番号 : 23580139
研究分野 : 農学
科研費の分科・細目 : 農芸化学・応用生物化学
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