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恶性疟原虫感染儿童的葡萄糖稳态:前体供应限制糖异生和葡萄糖生成。

Glucose homeostasis in children with falciparum malaria: precursor supply limits gluconeogenesis and glucose production.

作者信息

Dekker E, Hellerstein M K, Romijn J A, Neese R A, Peshu N, Endert E, Marsh K, Sauerwein H P

机构信息

Department of Internal Medicine, University of Amsterdam, The Netherlands.

出版信息

J Clin Endocrinol Metab. 1997 Aug;82(8):2514-21. doi: 10.1210/jcem.82.8.4131.

DOI:10.1210/jcem.82.8.4131
PMID:9253327
Abstract

To evaluate glucose kinetics in children with falciparum malaria, basal glucose production and gluconeogenesis and an estimate of the flux of the gluconeogenic precursors were measured in Kenyan children with uncomplicated falciparum malaria before (n = 11) and during infusion of alanine (1.5 mg/kg.min; n = 6). Glucose production was measured by [6,6-2H2]glucose, gluconeogenesis by mass isotopomer distribution analysis of glucose labeled by [2-13C]glycerol. Basal plasma glucose concentration ranged from 2.1-5.5 mmol/L, and basal glucose production ranged from 3.3-7.3 mg/kg.min. Glucose production was largely derived from gluconeogenesis (73 +/- 4%; range, 52-93%). During alanine infusion, plasma glucose increased by 0.4 mmol/L (P = 0.03), glucose production increased by 0.8 mg/kg.min (P = 0.02), and gluconeogenesis increased by 0.8 mg/kg.min (P = 0.04). We conclude that glucose production in children with uncomplicated falciparum malaria is largely dependent on gluconeogenesis. However, gluconeogenesis is potentially limited by insufficient precursor supply. These data indicate that in children with falciparum malaria, gluconeogenesis fails to compensate in the presence of decreased glycogen flux to glucose, increasing the risk of hypoglycemia.

摘要

为评估恶性疟原虫感染儿童的葡萄糖动力学,我们对肯尼亚患有非重症恶性疟原虫疟疾的儿童在输注丙氨酸前(n = 11)和输注丙氨酸期间(1.5 mg/kg·min;n = 6)测量了基础葡萄糖生成和糖异生,并估算了糖异生前体物质的通量。通过[6,6-2H2]葡萄糖测量葡萄糖生成,通过对用[2-13C]甘油标记的葡萄糖进行质量同位素异构体分布分析测量糖异生。基础血浆葡萄糖浓度范围为2.1 - 5.5 mmol/L,基础葡萄糖生成范围为3.3 - 7.3 mg/kg·min。葡萄糖生成主要来源于糖异生(73±4%;范围为52 - 93%)。在输注丙氨酸期间,血浆葡萄糖升高了0.4 mmol/L(P = 0.03),葡萄糖生成增加了0.8 mg/kg·min(P = 0.02),糖异生增加了0.8 mg/kg·min(P = 0.04)。我们得出结论,患有非重症恶性疟原虫疟疾的儿童的葡萄糖生成在很大程度上依赖于糖异生。然而,糖异生可能因前体物质供应不足而受到限制。这些数据表明,在患有恶性疟原虫疟疾的儿童中,在糖原向葡萄糖的通量降低的情况下,糖异生无法起到补偿作用,从而增加了低血糖的风险。

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Glucose homeostasis in children with falciparum malaria: precursor supply limits gluconeogenesis and glucose production.恶性疟原虫感染儿童的葡萄糖稳态:前体供应限制糖异生和葡萄糖生成。
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