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胰岛素和葡萄糖溶解对尼古丁胺胺 рибоoside 的心脏保护的依赖

Y Xiao^1,2,3, Q Wang^1,2, H Zhang^1,2

¹Amsterdam UMC, Laboratory of Experimental Intensive Care and Anesthesiology, Department of Anesthesiology, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.

Basic research in cardiology

|March 26, 2024

概括

尼古丁胺核糖化物 (NR) 通过激活糖分分解来保护心脏免受伤害,但当糖分分解已经高时,这种效果会消失,例如在胰岛素存在时.

科学领域:

心血管生物学心血管生物学
代谢调节代谢调节代谢调节
缺血-再输液损伤缺血-再输液损伤

背景情况:

尼古丁胺胺二核酸 (NAD+) 水平降低与疾病相关,包括衰老,糖尿病,心力衰竭和缺血-再输液损伤 (IRI).
尼古丁胺胺 рибоoside (NR),一个NAD+前体,显示治疗潜力,特别是减少心脏IRI. 然而,其保护机制和与胰岛素的相互作用仍然不清楚.

研究的目的:

调查NR是否能保护隔离的小鼠心脏免受IRI的影响.
阐明介导NR心脏保护作用的代谢途径.
确定胰岛素是否影响NR对心脏IRI的保护功效.

主要方法:

隔离的小鼠心脏在受控的代谢条件下 (轻度,无,或高糖解) 被 perfused.
心脏接受了IRI,并评估了NR对NAD+水平,心脏功能和代谢途径的影响.
代谢学和13C-葡萄糖流量学被用来分析代谢中间体和途径活动 (糖解,酸途径,TCA循环).

主要成果:

在所有代谢条件下,NR增加了心脏NAD+水平.
在心脏中NR降低了心脏IRI轻度糖解,与增加的糖解和特定的代谢中间体有关.
尽管NR增加了NAD+和一些中间体,但NR的保护作用在没有糖解或高糖解 (由胰岛素引起) 的心脏中丧失了.

结论:

NR对IRI的急性心脏保护取决于其激活糖解的能力.
当糖解已经高 (例如,用胰岛素) 或不存在时,这种保护作用会被废除.
这些发现凸显了糖解激活在NR介导心脏保护及其由胰岛素调节中的关键作用.

关键词:

葡萄糖溶解是什么? 葡萄糖溶解损伤 IR 损伤 IR 的情况.胰岛素是一种胰岛素.这就是为什么NAD+NAD+NAD.公共公共合作伙伴关系的途径.

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