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短期碳水化合物过量喂养期间碳水化合物耐受性的改善以及碳水化合物氧化和脂肪生成的刺激。

Improved carbohydrate tolerance and stimulation of carbohydrate oxidation and lipogenesis during short-term carbohydrate overfeeding.

作者信息

Welle S L, Campbell R G

出版信息

Metabolism. 1983 Sep;32(9):889-93. doi: 10.1016/0026-0495(83)90202-0.

Abstract

The carbohydrate intake of seven healthy men was increased from 220-265 g/d to 620-770 g/d for 17 days, while protein and fat intake remained constant. Carbohydrate loading did not affect the preprandial plasma glucose levels after an overnight fast, but reduced the postprandial increment in plasma glucose levels after 5, 11, and 17 days of overfeeding. Preprandial plasma insulin levels were slightly increased during carbohydrate overfeeding, but no increase in the postprandial rise in insulin levels was found until 11 days after the start of carbohydrate loading. Whole-body rates of carbohydrate oxidation and of glucose conversion to fat were estimated by indirect calorimetry. Basal carbohydrate oxidation rate was increased by 95% at the end of 17 days of overfeeding, but there was no potentiation in the stimulation of the carbohydrate oxidation rate induced by a meal. There was no net fat synthesis from glucose before carbohydrate loading; carbohydrate overfeeding produced nonprotein respiratory exchange ratios greater than 1.00, suggesting net fat synthesis from glucose. Meals did not stimulate net lipogenesis from glucose, either before or after overfeeding. These results indicate that the improvement in carbohydrate tolerance associated with short-term carbohydrate loading does not appear to depend on elevated insulin levels. Increased carbohydrate oxidation and lipogenesis elevated carbohydrate disposal is more than necessary to account for the improvement in carbohydrate tolerance.

摘要

7名健康男性的碳水化合物摄入量在17天内从220 - 265克/天增加到620 - 770克/天,而蛋白质和脂肪摄入量保持不变。碳水化合物负荷对禁食过夜后的餐前血浆葡萄糖水平没有影响,但在过量喂养5天、11天和17天后,降低了餐后血浆葡萄糖水平的升高。在碳水化合物过量喂养期间,餐前血浆胰岛素水平略有升高,但直到碳水化合物负荷开始11天后,餐后胰岛素水平的升高才被发现。通过间接测热法估计全身碳水化合物氧化率和葡萄糖转化为脂肪的速率。在过量喂养17天结束时,基础碳水化合物氧化率增加了95%,但进餐诱导的碳水化合物氧化率刺激没有增强。在碳水化合物负荷前,没有由葡萄糖净合成脂肪的情况;碳水化合物过量喂养产生的非蛋白呼吸商大于1.00,表明有由葡萄糖净合成脂肪的情况。无论在过量喂养前还是过量喂养后,进餐都不会刺激由葡萄糖的净脂肪生成。这些结果表明,与短期碳水化合物负荷相关的碳水化合物耐受性改善似乎不依赖于胰岛素水平升高。碳水化合物氧化增加和脂肪生成增加,碳水化合物处置增加,足以解释碳水化合物耐受性的改善。

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