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正常受试者口服葡萄糖后全身糖原沉积的机制。营养状况的影响。

Mechanisms of whole-body glycogen deposition after oral glucose in normal subjects. Influence of the nutritional status.

作者信息

Féry F, Plat L, Balasse E O

机构信息

Department of Endocrinology, Erasmus Hospital, University of Brussels, Belgium.

出版信息

J Clin Endocrinol Metab. 1998 Aug;83(8):2810-6. doi: 10.1210/jcem.83.8.5022.

Abstract

It is known that prior fasting enhances whole-body glycogen retention after glucose ingestion. To identify the involved mechanisms, 33 normal volunteers underwent a total fast, varying between 14 h and 4 days, and ingested thereafter 75 g glucose labeled with [14C]glucose. Measurements of oral glucose oxidation (expired 14CO2, corrected for incomplete recovery) and total carbohydrate (CHO) oxidation (indirect calorimetry) were performed over the following 5 h. These data allowed us to calculate oral glucose storage (uptake oxidation), glycogen oxidation (CHO oxidation - oral glucose oxidation), and net CHO balance (oral glucose uptake - CHO oxidation). As compared with an overnight fast, prolonged fasting (4 days) inhibited the uptake (64.8 vs. 70.3 g/5 h; P < 0.01) and the oxidation (10.9 vs. 20.0 g/5 h; P < 0.001) of oral glucose and stimulated slightly its conversion to glycogen (53.9 vs. 50.3 g/5 h; P < 0.05). The latter effect played only a minor role in the marked increase in net CHO balance (52.3 vs. 25.2 g/5 h; P < 0.001), which was almost entirely related to a decrease in glycogen oxidation (1.6 vs. 25.1 g/5 h; P < 0.001). Considering the whole series of data, including intermediate durations of fast, it was observed that the modifications in postprandial CHO metabolism, induced by fasting, correlated strongly with basal CHO oxidation, suggesting that the degree of initial glycogen depletion is a major determinant of glycogen oxidation and net CHO storage. Thus, prior fasting stimulates postprandial glycogen retention, mainly through an inhibition of the glycogen turnover that exists in overnight-fasted subjects, during the absorptive period.

摘要

已知空腹可增强葡萄糖摄入后全身糖原的留存。为明确其中涉及的机制,33名正常志愿者进行了14小时至4天不等的完全禁食,随后摄入75克用[14C]葡萄糖标记的葡萄糖。在接下来的5小时内测量口服葡萄糖氧化(呼出的14CO2,经不完全回收校正)和总碳水化合物(CHO)氧化(间接量热法)。这些数据使我们能够计算口服葡萄糖储存(摄取量 - 氧化量)、糖原氧化(CHO氧化 - 口服葡萄糖氧化)和净CHO平衡(口服葡萄糖摄取量 - CHO氧化)。与过夜禁食相比,长时间禁食(4天)抑制了口服葡萄糖的摄取(64.8对70.3克/5小时;P<0.01)和氧化(10.9对20.0克/5小时;P<0.001),并轻微刺激了其向糖原的转化(53.9对50.3克/5小时;P<0.05)。后一种效应在净CHO平衡的显著增加(52.3对25.2克/5小时;P<0.001)中仅起次要作用,净CHO平衡的增加几乎完全与糖原氧化的减少(1.6对25.1克/5小时;P<0.001)有关。考虑到包括中间禁食时长在内的整个数据集,观察到禁食引起的餐后CHO代谢变化与基础CHO氧化密切相关,这表明初始糖原耗竭程度是糖原氧化和净CHO储存的主要决定因素。因此,空腹主要通过抑制过夜禁食者在吸收期存在的糖原周转来刺激餐后糖原留存。

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