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Severe hypoglycemia exacerbates myocardial dysfunction and metabolic remodeling in diabetic mice

机译:严重的低血糖加剧了糖尿病小鼠的心肌功能障碍和代谢重塑

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摘要

Although several studies have revealed that adverse cardiovascular events in diabetic patients are closely associated with severe hypoglycemia (SH), the causal relationship and related mechanisms remain unclear. This study aims to investigate whether SH promotes myocardial injury and further explores the potential mechanisms with focus on disturbances in lipid metabolism. SH promoted myocardial dysfunction and structural disorders in the diabetic mice but not in the controls. SH also enhanced the production of myocardial proinflammatory cytokines and oxidative stress. Moreover, myocardial lipid deposition developed in diabetic mice after SH, which was closely related to myocardial dysfunction and the inflammatory response. We further found that myocardial metabolic remodeling was associated with changes in PPAR-beta/delta and its target molecules in diabetic mice exposed to SH. These findings demonstrate that SH exacerbates myocardial dysfunction and the inflammatory response in diabetic mice, which may be induced by myocardial metabolic remodeling via PPAR-beta/delta.
机译:虽然有几项研究表明,糖尿病患者的不良心血管事件与严重的低血糖症(SH)密切相关,但因果关系和相关机制仍然不明确。本研究旨在调查SH是否促进心肌损伤,并进一步探讨了富于脂质代谢的紊乱的潜在机制。 Sh在糖尿病小鼠中促进心肌功能障碍和结构障碍,但不在对照中。 SH还增强了心肌促炎细胞因子和氧化应激的产生。此外,在SH后在糖尿病小鼠中开发的心肌脂质沉积,其与心肌功能障碍和炎症反应密切相关。我们进一步发现,心肌代谢重塑与PPAR-Beta / delta的变化及其在暴露于SH的糖尿病小鼠中的靶分子有关。这些研究结果表明,SH加剧了心肌功能障碍和糖尿病小鼠的炎症反应,其可以通过PPAR-Beta / delta通过心肌代谢重塑诱导。

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