内科学
内分泌学
低血糖
葡萄糖摄取
胰岛素
败血症
生物
胰高血糖素
碳水化合物代谢
糖异生
回肠
基础(医学)
脾脏
新陈代谢
医学
作者
Charles H. Lang,C. Dobrescu
标识
DOI:10.1016/0026-0495(91)90048-2
摘要
The purpose of the present study was to determine how hypoglycemia alters glucose uptake by individual tissues and whether this response is altered by gram-negative infection. A hypermetabolic septic state was produced in catheterized rats by subcutaneous injections of live Escherichia coli. The next morning, animals were infused with saline, somatostatin to produce a euglycemic insulinopenic state (6 mmol/L glucose, 5 microU/mL insulin), or 3-mercaptopicolinate (3-MP) to inhibit gluconeogenesis and produce a hypoglycemic insulinopenic (4.5 or 2 mmol/L glucose, 5 microU/mL insulin) condition. After 140 minutes, [14C]2-deoxyglucose was injected intravenously (IV) to determine in vivo glucose uptake by individual tissues. Sepsis increased whole body glucose disposal (Rd) by 53% under basal euglycemic conditions and this increase resulted from an enhanced rate of glucose removal by liver, spleen, lung, ileum, and skin. Under euglycemic insulinopenic conditions, total glucose Rd decreased in both septic and nonseptic rats as a result of a decreased rate of glucose uptake by muscle. However, because the absolute rate of glucose uptake was still elevated by sepsis, the rate of non-insulin-mediated glucose uptake (NIMGU) was 46% higher in septic rats than in nonseptic animals. Severe hypoglycemia (2 mmol/L) produced a relative insulin deficiency and decreased whole body Rd in both septic and nonseptic animals by 53% to 58%, compared with euglycemic insulinopenic animals. The decrease in blood glucose decreased glucose uptake by all tissues examined, except brain and heart. However, sepsis still increased glucose uptake by liver, spleen, lung, ileum, and skin (25% to 90%), compared with hypoglycemic nonseptic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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