Stress Hyperglycemia in Critically Ill Patients: Insight Into Possible Molecular Pathways
Stress Hyperglycemia in Critically Ill Patients: Insight Into Possible Molecular Pathways
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DOI：
10.3389/fmed.2019.00054
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发表时间：
2019-03-27
影响因子：
3.9
通讯作者：
Brody, Edward
中科院分区：
文献类型：
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作者：
Bar-Or, David;Rael, Leonard T.;Brody, Edward
在非糖尿病患者中，严重脓毒症、全身炎症反应综合征(SIRS)和创伤性脑损伤经常与高血糖相关。在患有上述任何一种疾病的患者中，重症监护病房(ICU)入院时的高血糖与死亡率或发病率的增加直接相关。虽然最初对这些患者的血糖水平低于110 mg/dL的胰岛素治疗热情很高，但最近的理解表明，潜在的低血糖并发症使这种方法具有潜在的危险。更适度的血糖控制似乎比最初提出的积极降血糖更有益。一份重要的出版物表明，高乳酸血症伴随高血糖可能是不良结局的真正罪魁祸首。这表明，将适度降糖与可能治疗这些条件下潜在代谢紊乱的治疗药物结合起来可能是一种更好的策略。在这三种情况下，关键的代谢障碍似乎是持续的糖酵解作为能量来源，即使在组织充氧的情况下也是如此(Warburg效应)。我们综述了在理解有氧糖酵解和可能的DPP4对导致胰岛素失调的胰岛素的作用方面的最新进展，并提出了参与高血糖调节的关键代谢途径。
Severe sepsis, systemic inflammatory response syndrome (SIRS), and traumatic brain injury are frequently associated with hyperglycemia in non-diabetic patients. In patients suffering from any of these conditions, hyperglycemia at admission to an intensive care unit (ICU) is directly correlated with increased mortality or morbidity. Although there was initial enthusiasm for insulin treatment to blood glucose levels below 110 mg/dL in these patients, recent understanding suggests that the potential for hypoglycemic complications make this approach potentially dangerous. More moderate glucose control seems to be more beneficial than the aggressive glucose lowering initially suggested. An important publication has shown that hyperlactatemia accompanying hyperglycemia could be the real culprit in bad outcomes. This suggests that coupling moderate glucose lowering with therapeutic agents which might treat the underlying metabolic disturbances in these conditions may be a better strategy. The key metabolic disturbance in these three conditions seems to be persistent glycolysis as an energy source even in the presence of adequate tissue oxygenation (the Warburg Effect). We look at recent advances in understanding aerobic glycolysis and possibly the action of DPP4 on incretins resulting in insulin dysregulation and suggest key metabolic pathways involved in hyperglycemia regulation.