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首页> 外文期刊>Diabetes >Insulin-Induced Hypogiycemia and Its Effect on the Brain Unraveling Metabolism by In Vivo Nuclear Magnetic Resonance
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Insulin-Induced Hypogiycemia and Its Effect on the Brain Unraveling Metabolism by In Vivo Nuclear Magnetic Resonance

机译:胰岛素诱导的低氧血症及其对体内核磁共振的大脑解体代谢的影响

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摘要

Hypogiycemia, a frequent occurrence during modern intensive insulin therapy, remains the major limiting factor in achieving optimal glucose control in type 1 diabetic patients as well as in patients with long-standing type 2 diabetes. This has been a challenge for clinicians and investigators since several large population-based studies such as the Diabetes Control and Complications Trial and UK Prospective Diabetes Study established the long-term benefits of tight glycemic control many years ago (1,2). More recently, studies of intensive glucose control in patients with diabetes of several years duration have-to the surprise to many-been either terminated because of increased mortality in the intensive control arm or because worse outcomes were revealed in regard to the clinical end points (3,4). In a parallel development, we have gone, over the course of 10 years, from embracing stringent inpatient glucose control via insulin infusion protocols in the intensive care setting (5) to realizing that not everybody may benefit equally from such an intervention, since the increased incidence of profound hypogiycemia is the limiting factor (6). In fact, a recent systematic review of 21 trials of intensive insulin therapy by Kansagara et al. (7) found a sixfold higher risk of severe hypoglycemic events in patients undergoing such therapy. Faced with a clinical dilemma of such proportion, it appears that we may need to readdress our hypotheses, and we need to conduct mechanistic studies that allow us to identify therapies that are effective but minimize the exposure of patients to the heightened risk of hypogiycemia. Understanding the regulation of glucose metabolism in the brain and how it responds to hypogiycemia in this context is of particular relevance because of the brain's exquisite dependence on glucose as an energy substrate and its integrative function in whole body fuel homeostasis (8).
机译:低血糖症,在现代强化胰岛素治疗期间经常发生,仍然是实现1型糖尿病患者和长期2型糖尿病患者最佳血糖控制的主要限制因素。这对临床医生和研究人员来说一直是一个挑战,因为许多大型的基于人群的研究(例如糖尿病控制和并发症试验和英国前瞻性糖尿病研究)在多年前就确立了严格控制血糖的长期益处(1,2)。最近,对持续数年的糖尿病患者进行强化血糖控制的研究,令人惊讶的是,由于强化控制组死亡率的增加或临床终点的预后较差而终止研究( 3,4)。在平行发展中,我们已经走过了10年的时间,从在重症监护环境中接受通过胰岛素输注方案进行严格的住院葡萄糖控制(5)到意识到并非所有人都可以从这种干预中平等受益,因为严重低氧血症的发生是限制因素(6)。实际上,Kansagara等人最近对21种强化胰岛素治疗试验进行了系统综述。 (7)发现接受这种疗法的患者发生严重降血糖事件的风险高六倍。面对如此比例的临床难题,似乎我们可能需要重新阐明我们的假设,并且我们需要进行机制研究,以使我们能够确定有效的疗法,但可以最大程度地减少患者遭受低血氧血症的风险。在这种情况下,了解大脑中葡萄糖代谢的调控及其对低氧血症的反应具有特别重要的意义,因为大脑对葡萄糖作为能量底物的精细依赖及其在体内的稳态功能具有整合功能(8)。

著录项

  • 来源
    《Diabetes》 |2011年第7期|p.1856-1858|共3页
  • 作者单位

    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut;

    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut;

    Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, Connecticut;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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