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去甲肾上腺素和利钠肽在急性冠状动脉综合征患者葡萄糖利用中的协同作用。

Collaborative Activities of Noradrenaline and Natriuretic Peptide for Glucose Utilization in Patients with Acute Coronary Syndrome.

机构信息

Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.

出版信息

Sci Rep. 2019 May 24;9(1):7822. doi: 10.1038/s41598-019-44216-0.

Abstract

Glucose is an important preferential substrate for energy metabolism during acute coronary syndrome (ACS) attack, although insulin resistance (IR) increases during ACS. Increasing evidence indicates that natriuretic peptides (NP) regulate glucose homeostasis. We investigated possible compensatory actions of NP in collaboration with other neurohumoral factors that facilitate glucose utilization during ACS. The study population consisted of 1072 consecutive cases with ischemic heart disease who underwent cardiac catheterization (ACS, n = 216; non-ACS, n = 856). Among ACS subjects, biochemical data after acute-phase treatment were available in 91 cases, defined as ACS-remission phase (ACS-rem). Path models based on covariance structure analyses were proposed to clarify the direct contribution of B-type NP (BNP) and noradrenaline to glucose and HOMA-IR levels while eliminating confounding biases. In non-ACS and ACS-rem subjects, although noradrenaline slightly increased glucose and/or HOMA-IR levels (P < 0.03), BNP did not significantly affect them. In contrast, in ACS subjects, high noradrenaline was a significant cause of increases in glucose and HOMA-IR levels (P < 0.001), whereas high BNP was a significant cause of decreases in both parameters (P < 0.005). These findings indicate that BNP and noradrenaline coordinately activate glucose metabolism during ACS, with noradrenaline increasing glucose levels, as an energy substrate, while BNP improves IR and promotes glucose utilization.

摘要

葡萄糖是急性冠状动脉综合征 (ACS) 发作期间能量代谢的重要首选底物,尽管 ACS 期间会出现胰岛素抵抗 (IR)。越来越多的证据表明,利钠肽 (NP) 调节葡萄糖稳态。我们研究了 NP 与其他神经激素因素在 ACS 期间促进葡萄糖利用的可能代偿作用。研究人群包括 1072 例连续接受心脏导管检查的缺血性心脏病患者(ACS,n=216;非 ACS,n=856)。在 ACS 患者中,216 例患者中有 91 例在急性期治疗后可获得生化数据,定义为 ACS 缓解期(ACS-rem)。基于协方差结构分析提出了路径模型,以阐明 B 型利钠肽 (BNP) 和去甲肾上腺素对葡萄糖和 HOMA-IR 水平的直接贡献,同时消除混杂偏差。在非 ACS 和 ACS-rem 患者中,尽管去甲肾上腺素略微增加了葡萄糖和/或 HOMA-IR 水平(P<0.03),但 BNP 对其没有显著影响。相比之下,在 ACS 患者中,高去甲肾上腺素是葡萄糖和 HOMA-IR 水平升高的重要原因(P<0.001),而高 BNP 是这两个参数降低的重要原因(P<0.005)。这些发现表明,在 ACS 期间,BNP 和去甲肾上腺素协同激活葡萄糖代谢,去甲肾上腺素增加葡萄糖水平作为能量底物,而 BNP 改善 IR 并促进葡萄糖利用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb74/6534620/cb63d59000a9/41598_2019_44216_Fig1_HTML.jpg

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