简要回顾:缺血性卒中中的高血糖

Honglian Duan, Wesley Kohls, Roxanne Ilagan, Xiaokun Geng, Yuchuan Ding
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摘要

中风是目前世界上第二大死亡原因,其影响继续恶化,即使那些存活下来的人也可能有持续的神经功能缺陷。一个潜在的重大影响可能是由于高血糖,在三分之一的急性缺血性卒中(AIS)患者中发现。然而,先前的研究报告了关于高血糖对卒中后预后影响的相互矛盾的信息,可能是由于不同的应激性高血糖测量。葡萄糖与糖化血红蛋白比率是AIS后应激性高血糖的一个指标,它能更好地量化血糖的急性变化,而不是葡萄糖水平的绝对变化。适度的血糖降低可以抵消高血糖的负面影响,血糖控制药物也可以起到神经保护的作用。肝脏是维持能量和葡萄糖代谢的主要器官,AIS的作用可远及外周器官,包括肝脏。在这篇综述中,我们强调了急性卒中后高血糖的机制,这是一种肝脏炎症途径,可导致肝脏糖异生和肝脏胰岛素敏感性降低。肝炎级联导致肝脏糖异生,抗高血糖药物靶向治疗有可能改善脑卒中预后和恢复。
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Mini review: Hyperglycemia in ischemic stroke
The impact of stroke, currently the second leading cause of death worldwide, continues to worsen, and even those that survive can have persistent neurological deficits. A potentially significant implication may be due to hyperglycemia, found in one-third of all acute ischemic stroke (AIS) patients. However, prior studies reported conflicting information about the impact of hyperglycemia on poststroke prognosis, likely due to different measurements of stress-induced hyperglycemia. The glucose-to-glycated hemoglobin ratio is an index of stress-induced hyperglycemia after AIS that better quantifies acute changes in blood glucose, as opposed to absolute variations in glucose levels. Moderate blood glucose reductions might counteract the negative effects of hyperglycemia and glycemic control medications can also play a role in neuroprotection. The liver is the main organ that functions to maintain energy and glucose metabolism and the effects of AIS can reach far peripheral organs, including the liver. In this review, we highlighted the mechanism responsible for acute poststroke hyperglycemia, a hepatic inflammatory pathway that results in hepatic gluconeogenesis and reduced hepatic insulin sensitivity. Hepatitis cascades lead to hepatic gluconeogenesis, and targeted therapy with antihyperglycemic drugs has the potential to improve stroke prognosis and recovery.
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