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-β/δ 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-β/δ.

中文翻译：

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严重的低血糖症会加剧糖尿病小鼠的心肌功能障碍和代谢重构。

尽管多项研究表明，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，但其因果关系和相关机制仍不清楚。这项研究旨在调查SH是否促进心肌损伤，并进一步探讨潜在的机制，重点是脂质代谢紊乱。SH促进了糖尿病小鼠的心肌功能障碍和结构异常，但没有促进对照组的心肌功能异常和结构异常。SH还增强了心肌促炎细胞因子的产生和氧化应激。此外，SH后糖尿病小鼠的心肌脂质沉积发展，这与心肌功能障碍和炎症反应密切相关。我们进一步发现，心肌代谢重构与暴露于SH的糖尿病小鼠中PPAR-β/δ及其靶分子的变化有关。这些发现表明SH加重了糖尿病小鼠的心肌功能障碍和炎症反应，这可能是通过PPAR-β/δ引起的心肌代谢重塑而引起的。