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人体对2-脱氧-D-葡萄糖给药的体温调节及相关反应。

Thermoregulatory and related responses to 2-deoxy-D-glucose administration in humans.

作者信息

Thompson D A, Lilavivathana U, Campbell R G, Welle S L, Craig A B

出版信息

Am J Physiol. 1980 Sep;239(3):R291-5. doi: 10.1152/ajpregu.1980.239.3.R291.

Abstract

Hypothermia in humans during insulin-induced glucopenia has been largely attributed to impaired heat production. To further study the mechanism for hypothermia during glucoprivation six normal males were given 20-min intravenous infusions of 2-deoxy-D-glucose (2-DG), 50 mg/kg, a competitive inhibitor of glucose utilization. Oxygen and carbon dioxide exchange was measured to determine heat production by indirect calorimetry. Decreases in core temperature were initially associated with activation of mechanisms for heat loss such as sweating and hyperpnea 30-120 min after 2-DG infusion. Hypothermia persisted in spite of markedly increased plasma catecholamine, glucose, and free fatty acid levels from 60 to 180 min and increased heat production from 120 to 180 min after 2-DG infusion. Thus in contrast to the proposed mechanism for insulin-induced hypothermia, the hypothermia of 2-DG-induced glucoprivation is a consequence of increased heat loss and not of decreased heat production.

摘要

胰岛素诱导的低血糖期间人体体温过低主要归因于产热受损。为了进一步研究糖剥夺期间体温过低的机制,对6名正常男性静脉输注2 - 脱氧 - D - 葡萄糖(2 - DG),剂量为50mg/kg,输注时间为20分钟,2 - DG是一种葡萄糖利用的竞争性抑制剂。通过间接测热法测量氧气和二氧化碳交换以确定产热情况。输注2 - DG后30 - 120分钟,核心体温下降最初与散热机制的激活有关,如出汗和呼吸急促。尽管输注2 - DG后60至180分钟血浆儿茶酚胺、葡萄糖和游离脂肪酸水平显著升高,且120至180分钟产热增加,但体温过低仍持续存在。因此,与胰岛素诱导体温过低的推测机制相反,2 - DG诱导的糖剥夺引起的体温过低是散热增加的结果,而非产热减少的结果。

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