FGF1の内分泌は,ネオモルフで強力なインスリン感受剤を生成する
Jae Myoung Suh1, Johan W Jonker2, Maryam Ahmadian3
11] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2].
Nature
|July 22, 2014
まとめ
フィブロブラスト成長因子1 (FGF1) の投与は,糖尿病のマウスのグルコースを効果的に低下させます. この新しい治療法は,一般的な副作用なしにインスリン感受性を高め,2型糖尿病の治療に新たな希望をもたらします.
科学分野:
- メタボリック研究.
- エンドクリノロジー エンドクリノロジー
- 分子生物学は分子生物学である.
背景:
- フィブロブラスト成長因子1 (FGF1) は,主にオトクリン/パラクリンレギュレータであり,通常はタンパク質グリカンに結合し,循環を制限します.
- FGF1はミトゲン性特性で知られているが,栄養素ホメオスタシスにおけるFGF1の役割は,高脂肪食でFGF1をノックアウトしたマウスのインスリン抵抗性によって示唆されている.
研究 の 目的:
- インスリン抵抗性および2型糖尿病の管理における再結合FGF1 (rFGF1) の治療の可能性を調査する.
- FGF1の低血糖効果が,そのミトゲン性活動から分離できるかどうかを判断する.
主な方法:
- 糖尿病のマウスにrFGF1の単回投与を親腸内投与する.
- rFGF1.1による慢性薬理学的治療
- 血糖値の評価,インスリン依存性グルコース摂取量,肝臓のグルコース産生,体重増加や肝臓ステアトーシスなどの副作用.
- FGF受容体1の信号伝達経路の分析.
主要な成果:
- rFGF1の単一投与は,低血糖を引き起こすことなく,強力で,投与量に依存し,インスリンに依存したグルコース低下を誘発しました.
- 慢性的なrFGF1治療は,骨格筋のグルコース吸収を増加させ,肝臓のグルコース生産を減少させることで全身のインスリン感受性を改善しました.
- rFGF1治療は,体重増加,肝臓ステアトーシス,または骨減少などの副作用をもたらしませんでした.
- 血糖を下げる効果は,主にFGF受容体1シグナル伝達によって媒介されるミトゲン活性から分離された.
結論:
- 外因的,非ミトジェニックのFGF1は,新種のインスリン感受性作用を示し,インスリン抵抗性および2型糖尿病の治療の可能性を持っています.
- FGF1は,代謝障害に対する有望な治療薬であり,現在の治療の副作用なしに利点を提供します.
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