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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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アスプロシン,断食誘発型グルコゲンタンパク質ホルモン
Chase Romere1, Clemens Duerrschmid1, Juan Bournat1
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Cell
|April 19, 2016
まとめ
研究者はアスプロシンという 禁食によるタンパク質ホルモンを発見し 肝臓のグルコースの放出を増加させました アスプロシン濃度を下げると,インスリン抵抗性の患者でグルコースとインスリンが有意に低下し,II型糖尿病の治療が可能となる.
科学分野:
- 代謝の調節
- 内分泌学
- 分子生物学
背景:
- 肝臓からのグルコースの放出は,特に断食中に,血糖の恒常性を維持するために極めて重要です.
- ホルモンの調節は精密に血糖値を制御します.
- 肝臓のグルコース調節における特定の断食誘発ホルモンの役割については,さらなる解明が必要である.
研究 の 目的:
- 肝臓のグルコースの放出を調節する新しい断食誘発ホルモンを特定し,特徴づけること.
- 特定されたホルモンの作用機構を調査する.
- 代謝障害におけるこのホルモンの治療の可能性を評価する.
主な方法:
- プロフィブリリン分裂による新しいタンパク質ホルモン (アスプロシン) の特定.
- 人間とマウスの循環中のアスプロシン濃度の測定
- 肝臓におけるアスプロシンのシグナル伝達経路 (Gタンパク質-cAMP-PKA) の調査
- 免疫学的または遺伝的アブレーション後のグルコースとインスリンレベルに対するAsprosinの効果の評価
主要な成果:
- アスプロシンはプロフィブリリンのC端割れ産物で,白い脂肪組織によって分泌されます.
- アスプロシンは肝臓におけるGタンパク質- cAMP- PKA経路を活性化し,グルコースの放出を刺激する.
- インスリン抵抗性のヒトとマウスでは,病理的に上昇したアスプロシン濃度が観察されています.
- アスプロシン機能の喪失は,肝臓のグルコースの放出が低下したため,グルコースとインスリンが著しく減少する.
結論:
- アスプロシンは,肝臓のグルコースの放出を調節する重要な役割を果たす新しいグルコゲンタンパク質ホルモンです.
- アスプロシンの治療標的は,II型糖尿病と代謝症候群の管理に有望な戦略を提供することができる.
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