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糖尿病酮症酸中毒期间的丙酮代谢

Acetone metabolism during diabetic ketoacidosis.

作者信息

Owen O E, Trapp V E, Skutches C L, Mozzoli M A, Hoeldtke R D, Boden G, Reichard G A

出版信息

Diabetes. 1982 Mar;31(3):242-8. doi: 10.2337/diab.31.3.242.

Abstract

The presence and the importance of acetone and its metabolism in diabetic ketoacidosis has largely been ignored. Therefore, we studied acetone metabolism in nine diabetic patients in moderate to severe ketoacidosis. The concentration of acetone in plasma, urine, and breath, and the rates of acetone production and elimination in breath and urine were determined and the rates of vivo metabolism were calculated. Plasma acetone concentrations (1.55-8.91 mM) were directly related and were generally greater than acetoacetate concentrations (1.16-6.08 mM). The rates of acetone production ranged from 68 to 581 mumol/min/1.73 m2, indicating the heterogeneous nature of the patients studied. The average acetone production rate was 265 mumol/min/1.73 m2 and accounted for about 52% of the estimated acetoacetate production rate. Urinary excretion of acetone remained constant and accounted for about 7% of the acetone production rate in all patients. There was a positive linear relationship between the percentage of the acetone production rate accounted for by excretion in breath and the plasma acetone concentration. At low plasma acetone concentrations, approximately 20%, and at high plasma acetone concentrations, approximately 80% of the production rate was accounted for by breath acetone. In contrast, there was a negative linear relationship between the percentage of acetone production rate undergoing in vivo metabolism and plasma acetone concentration. At low plasma acetone concentrations, approximately 75%, and at high concentrations, approximately 20% of acetone production rate was accounted for by in vivo metabolism. Radioactivity from 2-[14C]-acetone was variably present in plasma acetone, glucose, lipids and proteins. No radioactivity was found in plasma acetoacetate, beta-hydroxy butyrate or free fatty acids or other anionic compounds. Exchange rates of acetone into other metabolites could not be estimated because of non-steady-state precursor product relationships in these patients.

摘要

丙酮及其代谢在糖尿病酮症酸中毒中的存在情况和重要性在很大程度上被忽视了。因此,我们研究了9例中度至重度酮症酸中毒糖尿病患者的丙酮代谢情况。测定了血浆、尿液和呼出气体中丙酮的浓度,以及呼出气体和尿液中丙酮的生成和消除速率,并计算了体内代谢速率。血浆丙酮浓度(1.55 - 8.91 mM)呈直接相关,且一般高于乙酰乙酸浓度(1.16 - 6.08 mM)。丙酮生成速率范围为68至581 μmol/min/1.73 m²,表明所研究患者的异质性。丙酮平均生成速率为265 μmol/min/1.73 m²,约占估计乙酰乙酸生成速率的52%。所有患者中,丙酮的尿排泄量保持恒定,约占丙酮生成速率的7%。呼出气体中丙酮排泄量占丙酮生成速率的百分比与血浆丙酮浓度呈正线性关系。在血浆丙酮浓度较低时,约20%的生成速率由呼出气体中的丙酮所致;在血浆丙酮浓度较高时,约80%的生成速率由呼出气体中的丙酮所致。相反,体内代谢的丙酮生成速率百分比与血浆丙酮浓度呈负线性关系。在血浆丙酮浓度较低时,约75%的丙酮生成速率由体内代谢所致;在浓度较高时,约20%的丙酮生成速率由体内代谢所致。2-[¹⁴C]-丙酮的放射性在血浆丙酮、葡萄糖、脂质和蛋白质中呈可变存在。在血浆乙酰乙酸、β-羟基丁酸或游离脂肪酸或其他阴离子化合物中未发现放射性。由于这些患者中前体产物关系处于非稳态,无法估计丙酮与其他代谢物的交换速率。

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