肥満における心筋活力学: ストレス反応の鈍化によるクレアチンキナーゼによるATP供給の強化
Jennifer J Rayner1, Mark A Peterzan1, William D Watson1
1Oxford Centre for Clinical Magnetic Resonance Research, Division of Cardiovascular Medicine, Radcliffe Department of Medicine (J.J.R, M.A.P., W.D.W., S.N., O.J.R.), University of Oxford, John Radcliffe Hospital, United Kingdom.
Circulation
|March 7, 2020
まとめ
肥満では心臓が
科学分野:
- 心臓病科
- 代謝障害
- バイオ物理学
背景:
- 肥満は運動不耐症と 心不全に関連しています
- 肥満では心筋動脈のエネルギーと腹動脈の機能が低下するが,通常は心筋動脈の機能が維持される.
- 肥満の心臓のATP供給メカニズムは まだ十分に研究されていません
研究 の 目的:
- ヒトの肥満におけるクレアチンキナーゼ (CK) 経由による心筋ATP伝達率を調査する.
- CKの活性が増加して,静止状態のフォスフォクレアチン (PCr) / ATPのレベルが低下することを補償するかどうかを判断する.
- これらのエネルギー変化が体重減少で正常化するか調べる.
主な方法:
- 80人のボランティア (対照群35人,肥満者45人) は,体質分析,MRI,31P磁気共鳴光譜検査を受けた.
- 静止状態のフォスフォクレアチン/ATPとドブタミンストレス中のCK運動を評価した.
- 肥満の参加者は減量介入と再評価を受けた.
主要な成果:
- 肥満の心臓は静止中の心筋フォスフォクレアチン/ATPが低かったが,静止中のATP供給を維持するCK反応率が高かった.
- 対照群では,ストレス中にCK活動とATPの放出が増加したが,肥満の心臓ではそうではなかった.
- 肥満者におけるシストリック増幅の減少は,ストレス時のエネルギー供給の低下と相関する.
- 体重減少は 筋肉のエネルギー異常を 正常化させました
結論:
- 肥満における心筋CK活性の増加は,休息時のATP供給を維持するが,ストレス時の増強を制限する.
- 心筋のエネルギー供給の障害は,肥満における運動耐性の低下に寄与する.
- 体重減少はこれらの有害な心臓のエネルギー適応を逆転させます
- CKのような心筋エネルギー経路をターゲットにすることで 肥満に関連した心臓病の治療効果が得られます
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