禁食を模倣するダイエットは,NGN3-駆動β細胞再生を促し,糖尿病を逆転させます
Chia-Wei Cheng1, Valentina Villani2, Roberta Buono3
1Longevity Institute, School of Gerontology, Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA; Koch Institute at MIT, 500 Main Street, Cambridge, MA 02139, USA.
Cell
|February 25, 2017
まとめ
禁食を模倣するダイエット (FMD) は,マウスと人間の臓細胞のインスリン生成細胞を再生することができます. この食事介入は,グルコースホメオスタシスとインスリン分泌を回復することによって,タイプ1とタイプ2の糖尿病を逆転させる可能性を示しています.
科学分野:
- 代謝疾患
- 再生医療
- 内分泌学
背景:
- 幹細胞治療は 臓器再生の可能性を秘めていますが 組織除去や 再生プログラムを開始する際に 課題に直面しています
- 1型と2型を含む糖尿病は,インスリン生産の低下とグルコースの調節不全によって特徴付けられます.
研究 の 目的:
- 禁食模倣ダイエット (FMD) が臓細胞の再プログラムと再生を誘発する可能性を調査する.
- 糖尿病の臨床前モデルとヒトの臓小島におけるインスリン分泌とグルコースホメオスタシスの回復におけるFMDの有効性を評価する.
主な方法:
- 1型および2型糖尿病のマウスモデルに4日間の断食模倣ダイエット (FMD) を投与した.
- 遺伝子発現分析 (Sox17,Pdx-1,Ngn3,Sox2) はマウスとヒトの臓小島で実施された.
- インスリン生成とグルコースホメオスタシスを評価した.
- PKAとmTORのシグナル伝達経路の阻害と,IGF-1治療と併用して,口腔炎の効果を調べた.
主要な成果:
- マウスはSox17, Pdx-1, Ngn3を段階的に発現させ,インスリン産生ベータ細胞の生成を促進した.
- 1型糖尿病と2型糖尿病のマウスモデルにおいて,FMDサイクルはインスリン分泌とグルコースホメオスタシスを回復させた.
- ヒトの1型糖尿病群島では,断食によりPKAとmTORの活性が低下し,Sox2,Ngn3の発現とインスリン生成が増加し,PKA/mTORの抑制によって模倣され,IGF-1によって逆転した.
結論:
- 禁食を模倣したダイエットは インスリン生成を回復する 臓細胞の再プログラムを促進します
- マウスモデルでは1型および2型糖尿病の表型を逆転させる可能性が示されています.
- 糖尿病に対する新たな治療戦略として,内生的な再生能力を高めることが可能である.
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