アセタートは,メタボリックシンドロームを促進する微生物群-脳-β細胞軸を媒介する
Rachel J Perry1, Liang Peng1, Natasha A Barry2,3
1Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Nature
|June 10, 2016
まとめ
変化した腸内微生物群は アセテットを増加させ 肥満を促す神経系を活性化させます この栄養素と腸の相互作用と 神経系の活性化は 肥満の治療の標的となる可能性があります
科学分野:
- 微生物学
- 神経科学
- 代謝に関する研究
背景:
- 肥満,インスリン抵抗性,代謝症候群は腸内微生物の変化と関連しています.
- 腸内微生物群の変化とこれらの状態を結びつける正確なメカニズムは不明です.
研究 の 目的:
- 腸内微生物群の変異が肥満および関連する代謝状態に寄与するメカニズムを調査する.
主な方法:
- 変異した腸内微生物群とアセテット生成の影響を研究するために,ネズミのモデルを使用した.
- 腸内微生物群の変化を媒介する 寄生神経系の役割を調査した.
主要な成果:
- 変異した腸内微生物群によるアセテット産生の増加は 副交感神経系を活性化させます
- この活性化により,グルコース刺激によるインスリン分泌,グレーリン分泌,および過食が増加します.
- 歯類における観察された効果は,肥満および関連する代謝的後遺症に寄与する.
結論:
- 栄養素と腸内微生物の相互作用によるアセテート生成の増加と,その後のパラシンパティック活性化は,肥満の発症の重要なメカニズムである.
- アセテット生成とパラシンパティック活性化をターゲットにすることで,肥満に対する潜在的な治療戦略を提示します.
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